Cardiovascular | Blood Pressure Regulation | Hypotension

Compensation Mechanisms for Low Blood Pressure

In this section, the speaker discusses compensation mechanisms that occur in the body when experiencing low blood pressure. The focus is on understanding how the body compensates to bring blood pressure back up.

Understanding Low Blood Pressure

• Hypotension, or low blood pressure, is classified when the systolic blood pressure (ventricular pressure) falls below 100 mmHg.

• Compensation mechanisms are triggered when blood pressure drops below 100 mmHg.

Baroreceptors and Detection of Blood Pressure Changes

• Baroreceptors are pressure receptors that detect changes in blood pressure.

• Two locations where baroreceptors are found: aortic sinus and carotid sinus.

• Aortic Sinus: Contains baroreceptors carried by cranial nerve 10 (vagus nerve).

• Carotid Sinus: Contains baroreceptors carried by cranial nerve 9 (glossopharyngeal nerve).

Response of Baroreceptors to Blood Pressure Changes

• When blood vessel walls stretch due to high blood pressure, it activates channels on the sensory nerve endings of baroreceptors.

• Activation of these channels allows sodium ions to flow in.

Classification of Low Blood Pressure

This section focuses on classifying low blood pressure and provides specific criteria for hypotension.

Criteria for Hypotension

• Systolic blood pressure less than 100 mmHg is classified as hypotension.

• Hypotension can be significantly lower, even down to around 80 mmHg in certain situations like hypovolemic shock.

Compensation Mechanisms for Low Blood Pressure

This section continues discussing compensation mechanisms that occur when blood pressure drops below 100 mmHg.

Role of Baroreceptors in Compensation

• Baroreceptors in the aortic sinus and carotid sinus detect changes in blood pressure.

• Information from baroreceptors is carried by cranial nerves 10 (vagus nerve) and 9 (glossopharyngeal nerve).

• The information is transmitted to the nucleus of tractus solitarius, a special nucleus in the medulla.

Location of Baroreceptors

This section explains the specific locations where baroreceptors are found.

Aortic Sinus

• Baroreceptors are located in the aortic sinus, which is part of the aorta.

• These baroreceptors detect changes in blood pressure within the aorta.

• Carried by cranial nerve 10 (vagus nerve).

Carotid Sinus

• Baroreceptors are located at the bifurcation point of the left common carotid artery.

• These baroreceptors detect changes in blood pressure within the carotid artery.

• Carried by cranial nerve 9 (glossopharyngeal nerve).

Function of Baroreceptors

This section explains how baroreceptors respond to changes in blood pressure.

Activation of Baroreceptor Channels

• When blood vessel walls stretch due to high blood pressure, it activates channels on sensory nerve endings of baroreceptors.

• Activation allows sodium ions to flow into these channels.

Sensory Nerve Endings and Cranial Nerves

This section discusses sensory nerve endings connected to baroreceptor function and their associated cranial nerves.

Aortic Sinus Sensory Nerve Endings

• Sensory afferent fibers from sensory nerve endings in the aortic sinus are carried by cranial nerve 10 (vagus nerve).

Carotid Sinus Sensory Nerve Endings

• Sensory afferent fibers from sensory nerve endings in the carotid sinus are carried by cranial nerve 9 (glossopharyngeal nerve).

Sodium Ion Flow and Blood Pressure

This section explains how sodium ion flow is related to blood pressure changes.

Sodium Ion Flow Mechanism

• When blood vessel walls stretch, sodium ions flow into the channels of baroreceptor sensory nerve endings.

• This mechanism is activated when blood pressure is high.

The transcript does not provide further information beyond this point.

New Section

This section discusses the impact of low blood pressure on action potentials and the stimulation of the vagus nerve.

Impact of Low Blood Pressure

• When blood pressure is low, there is minimal or slow occurrence of action potentials in nerves.

• Low blood pressure results in little stretch on the blood vessel wall, inhibiting the sensory afferent fibers of the vagus nerve.

• The sensory afferent fibers of the Bair receptors in the carotid sinus are also inhibited.

• The nucleus of tractus solitarius receives this information and determines the appropriate response.

New Section

This section explains the different centers involved in regulating blood pressure.

Centers Regulating Blood Pressure

• The maroon center, known as the cardiac accelerator center (CA), is connected to the sympathetic nervous system.

• The brown center, called the vasomotor center (VM), is also connected to the sympathetic nervous system.

• The green center, known as the cardiac inhibitory center, houses the dorsal nucleus of Vegas and is connected to the parasympathetic nervous system.

• These centers receive signals from glossopharyngeal and vagus nerves at the nucleus of tractus solitarius.

New Section

This section explores how different centers respond to low blood pressure.

Response to Low Blood Pressure

• Signals from glossopharyngeal and vagus nerves reach three centers: cardiac accelerator center, cardiac inhibitory center, and vasomotor center.

• To increase blood pressure:

• Stimulate cardiac accelerator center to increase heart rate and stroke volume, thereby increasing cardiac output.

• Inhibit cardiac inhibitory center to prevent slowing down heart rate.

• Stimulate vasomotor center to activate sympathetic nervous system and constrict blood vessels, increasing total peripheral resistance.

New Section

This section discusses the relationship between blood pressure and cardiac output.

Blood Pressure and Cardiac Output

• Blood pressure is determined by the formula: blood pressure = cardiac output * total peripheral resistance.

• To increase cardiac output:

• Increase heart rate through stimulation of the cardiac accelerator center.

• Increase stroke volume.

• To increase total peripheral resistance:

• Constrict blood vessels through activation of the vasomotor center.

• Increasing cardiac output and total peripheral resistance leads to an increase in blood pressure.

New Section

This section explains the sympathetic outflow region in the spinal cord involved in regulating blood pressure.

Sympathetic Outflow Region

• The activated cardiac accelerator center sends signals to a specific region in the spinal cord, ranging from T1 to L2.

• This region is known as the sympathetic outflow, which controls sympathetic nervous system activity related to blood pressure regulation.

New Section

This section discusses the pathways of ganglion and their destinations within the heart.

Pathways of Ganglion and Their Destinations

• Ganglion travel to two destinations within the heart.

• One destination is a special structure located within the right atrium.

• The other destination is located near the bifurcation where the atria and ventricles are separated.

• These two areas are known as the SA node and AV node.

• Chemicals released by ganglion onto these nodes include norepinephrine, which binds to beta-1 adrenergic receptors.

• Activation of these receptors stimulates a G-protein, adenylate cyclase, which converts ATP into cyclic AMP (cAMP).

• cAMP activates protein kinase A, which phosphorylates channels on the membrane, allowing excessive calcium influx into the SA node and AV node.

• Increased calcium influx leads to more action potentials and an increased heart rate.

• An increased heart rate ultimately increases cardiac output and blood pressure.

New Section

This section explores how sympathetic nerves can also affect the myocardium of the heart.

Sympathetic Nerves' Effect on Myocardium

• Sympathetic nerves can also target the myocardium of the heart in addition to acting on nodal cells like SA node and AV node.

• The mechanism of action is similar, involving cyclic AMP (cAMP) activation through protein kinase A.

• Calcium flows into myocardial cells upon cAMP activation, leading to increased cross bridge formation between actin and myosin filaments.

• More cross bridges result in a more powerful contraction of the myocardium.

New Section

This section explains how increased calcium levels lead to more cross bridges between actin and myosin filaments, resulting in a more powerful contraction.

Increased Calcium and Cross Bridge Formation

• Increased calcium levels in the myocardium lead to the binding of calcium to troponin.

• This binding changes the shape of tropomyosin, exposing active sites for myosin to bind with actin.

• More cross bridges between actin and myosin filaments allow for a more powerful contraction of the myocardium.

New Section

This section summarizes how increased calcium levels result in more cross bridges and a stronger contraction of the myocardium.

Summary: Increased Calcium and Stronger Contraction

• Higher calcium levels facilitate more cross bridge formation between actin and myosin filaments.

• More cross bridges lead to a stronger contraction of the myocardium.

Sympathetic Nervous System and Blood Pressure Regulation

In this section, the speaker discusses the role of the sympathetic nervous system in regulating blood pressure.

Activation of Sympathetic Nervous System on Heart

• The sympathetic nervous system acts on the SA node, AV node, and myocardium of the heart.

• Protein kinase A is involved in this process, phosphorylating calcium channels and increasing calcium flow.

• The overall effect is an increase in heart rate and contractility, leading to an increase in blood pressure.

Vasomotor Center and Blood Vessel Constriction

• The vasomotor center is stimulated by the nucleus of tractus solitarius.

• Fibers from the vasomotor center go to preganglionic neurons located within the spinal cord.

• These fibers then go to ganglia located near blood vessels.

• The fibers terminate in the tunica media (muscular layer) of arterioles.

• Activation of alpha one adrenergic receptors by norepinephrine leads to smooth muscle contraction and vasoconstriction.

• Vasoconstriction increases total peripheral resistance, resulting in increased blood pressure.

Role of Adrenal Medulla

• Special sympathetic fibers pass through sympathetic chain ganglia to reach the adrenal medulla.

• These fibers synapse on chromaffin cells within the adrenal medulla.

• Chromaffin cells release epinephrine (80%) and norepinephrine (20%).

• Epinephrine and norepinephrine have similar effects as other sympathetic neurotransmitters on blood vessels.

Summary: Sympathetic Nervous System's Influence on Blood Pressure

This section provides a summary of the key points discussed regarding the influence of the sympathetic nervous system on blood pressure regulation.

• The sympathetic nervous system plays a crucial role in regulating blood pressure.

• Activation of the sympathetic nervous system leads to increased heart rate and contractility, resulting in increased blood pressure.

• The vasomotor center stimulates vasoconstriction, which further increases blood pressure by increasing total peripheral resistance.

• The adrenal medulla releases epinephrine and norepinephrine, which have similar effects on blood vessels as other sympathetic neurotransmitters.

New Section

This section discusses the role of kidneys in regulating blood pressure and the release of renin.

The Role of Kidneys in Blood Pressure Regulation

• The kidneys have their own auto-regulation mechanism to protect themselves during changes in blood pressure.

• Special cells called JG cells in the kidney respond to low blood pressure by releasing a chemical called renin.

• Renin is released into the bloodstream and acts on angiotensinogen, an inactive protein produced by the liver.

• Renin cleaves angiotensinogen, converting it into angiotensin 1.

• Angiotensin 1 continues through the blood process until it reaches the lungs where it encounters angiotensin converting enzyme (ACE).

• ACE converts angiotensin 1 into a powerful hormone called angiotensin 2.

Actions of Angiotensin 2

• Angiotensin 2 stimulates zona glomerulosa cells in the adrenal cortex to release aldosterone, a hormone involved in fluid and electrolyte balance.

• Angiotensin 2 also acts on receptors in the hypothalamus and pituitary gland, leading to various physiological effects.

New Section

This section explores the actions of angiotensin 2 on different parts of the body.

Actions of Angiotensin 2 Continued

• Angiotensin 2 stimulates zona glomerulosa cells to release aldosterone, which affects fluid and electrolyte balance.

• Angiotensin 2 also acts on receptors in the hypothalamus and pituitary gland, leading to various physiological effects.

The transcript does not provide further information beyond this point.

New Section

This section discusses the activation of the super optic nucleus and the release of antidiuretic hormone (ADH) into the bloodstream. It also mentions the neurons in the hypothalamus that control thirst.

Activation of Super Optic Nucleus and Release of ADH

• The super optic nucleus is activated, triggering the release of ADH into the bloodstream. ADH is also known as vasopressin.

• ADH increases water absorption across the gastrointestinal tract, leading to increased blood volume and end diastolic volume. This results in an increase in stroke volume, cardiac output, and blood pressure.

Neurons Controlling Thirst

• Neurons located within the hypothalamus control thirst. Angiotensin II stimulates these neurons, leading to the release of chemicals that trigger thirst.

• Increased thirst leads to increased water intake, which results in increased fluid absorption across the GI tract and further increases blood volume, end diastolic volume, stroke volume, cardiac output, and blood pressure.

New Section

This section focuses on how ADH acts on the kidney's nephron to regulate water reabsorption.

Action of ADH on Collecting Duct

• ADH acts on V2 receptors in the collecting duct of nephrons.

• When ADH binds to its receptor, it activates a G stimulatory protein that triggers a cascade leading to increased levels of cyclic AMP (cAMP) and protein kinase A (PKA).

• PKA phosphorylates vesicles containing aquaporin 2 proteins.

• Phosphorylation triggers fusion between vesicles and the membrane, allowing aquaporin 2 channels to be inserted into the membrane.

• Water flows through these aquaporin 2 channels, increasing water reabsorption from the kidney tubules into circulation. This increases blood plasma volume, blood volume, end diastolic volume, stroke volume, cardiac output, and blood pressure.

Action of ADH on Distal Convoluted Tubules

• ADH also acts on the distal convoluted tubules.

• Aldosterone is another hormone that acts on this area.

• The exact mechanism of action for ADH and aldosterone in the distal convoluted tubules is not mentioned in the transcript.

New Section

This section discusses how aldosterone acts on specific areas of the kidney to regulate water and sodium reabsorption.

Action of Aldosterone on Distal Convoluted Tubules

• Aldosterone binds to receptors in the nucleus of cells in the distal convoluted tubules.

• The exact mechanism by which aldosterone affects water and sodium reabsorption in this area is not mentioned in the transcript.

The transcript does not provide further information about other aspects related to aldosterone's actions or any additional topics beyond what has been summarized above.

New Section

This section discusses the main proteins involved in the regulation of sodium and potassium channels in the kidneys.

Main Proteins and Their Functions

• The main protein responsible for regulating sodium channels is located in the basolateral membrane.

• Another protein is responsible for regulating potassium channels, allowing potassium ions to leak out.

• A pump located in the cell membrane pumps three sodium ions out of the cell and two potassium ions into the cell using ATP.

New Section

This section explains how the regulation of sodium and water absorption affects blood pressure.

Regulation of Sodium and Water Absorption

• ADH hormone acts on V2 receptors, increasing cyclic AMP pathway and expression of aquaporin type 2, leading to water absorption.

• Increased water volume inside the bloodstream leads to increased blood plasma volume, blood volume, end diastolic volume, stroke volume, cardiac output, and ultimately blood pressure.

New Section

This section discusses additional effects of angiotensin II on kidney function.

Effects of Angiotensin II

• Angiotensin II can bind to receptors present on proximal convoluted tubule cells, increasing reabsorption of sodium chloride and water.

• Increased reabsorption leads to increased blood volume, end diastolic volume, stroke volume, cardiac output, and blood pressure.

• Angiotensin II can also bind to receptors on arterioles' tunica media causing vasoconstriction and further increasing blood pressure.

New Section

This section explains the relationship between blood flow to the kidneys, urine output, and blood pressure.

Blood Flow, Urine Output, and Blood Pressure

• Low blood flow to the kidneys due to low blood pressure results in decreased urine output.

• Decreased urine output helps maintain fluid volume within the blood to preserve blood pressure.

• A decrease in glomerular filtration rate leads to decreased urine output.

New Section

This section mentions how the cortex and limbic nuclei can influence blood pressure.

Influence of Cortex and Limbic Nuclei

• The cortex has influence over respiratory centers and hypothalamus, which can control blood pressure.

• Special nuclei called limbic nuclei can also influence respiratory centers.

New Section

This section discusses the influence of limbic nuclei, hypothalamus, and cerebral cortex on the medullary cardiovascular and vasomotor centers.

Influence of Brain Structures on Cardiovascular Centers

• The limbic nuclei, hypothalamus, and even parts of the cerebral cortex have some influence on the medullary cardiovascular and vasomotor centers.

New Section

In this section, we learn about compensation mechanisms when blood pressure is too high.

Compensation Mechanisms for High Blood Pressure

• The next video will cover the compensation mechanisms that come into play when our blood pressure is too high.

• We will explore how this cell is used in regulating high blood pressure.