Cardiovascular | Blood Pressure Regulation | Hypertension

What Happens When Blood Pressure is Too High

In this video, the speaker discusses the effects of high blood pressure on the body and how it triggers compensation mechanisms. The term used for high blood pressure is hypertension, which is defined as systolic blood pressure greater than 140 mmHg or diastolic blood pressure greater than 90 mmHg.

Understanding Hypertension

• Hypertension refers to high blood pressure, with systolic blood pressure above 140 mmHg or diastolic blood pressure above 90 mmHg.

• Systolic hypertension occurs when the systolic blood pressure exceeds 140 mmHg.

• Diastolic hypertension occurs when the diastolic blood pressure exceeds 90 mmHg.

Baroreceptors and Compensation Mechanisms

• Baroreceptors are structures in our body that respond to changes in blood pressure.

• There are baroreceptors located in the carotid sinus (cranial nerve IX - glossopharyngeal nerve) and aortic sinus (cranial nerve X - vagus nerve).

• These baroreceptors send information to the nucleus of tractus solitarius (NTS), located in the medulla.

• Increased stretch due to high blood pressure activates sodium channels on sensory afferent nerve endings of baroreceptors.

• Sodium influx depolarizes the sensory afferent nerve endings, leading to action potentials being sent via cranial nerves IX and X to the NTS in the medulla.

Response within Medulla

• The NTS sends signals to three different centers within the medulla, including the cardiac center.

• (Timestamp not provided in transcript) The activation of these centers leads to various compensatory responses to regulate blood pressure.

Conclusion

The video provides an overview of what happens when blood pressure is too high (hypertension). It explains how baroreceptors detect changes in blood pressure and trigger compensation mechanisms through the medulla. Understanding these processes is crucial for managing hypertension effectively.

New Section

This section discusses the C1 and A1 areas of the vasomotor center, their functions, and how they are affected by blood pressure.

C1 Area and A1 Area

• The C1 area is responsible for constriction of blood vessels, while the A1 area is responsible for vasodilation.

• The C in C1 can be remembered as "constriction," and the A in A1 can be remembered as "vasodilation."

• In low blood pressure situations, the C1 area is inhibited and the A1 area is stimulated.

• In high blood pressure situations, it is important to inhibit the cardiac excitatory center to avoid further increase in heart rate and blood pressure.

New Section

This section explains how the vasomotor center and cardiac inhibitory center are connected with the parasympathetic nervous system.

Cardiac Inhibitory Center

• The cardiac inhibitory center is part of the parasympathetic nervous system.

• It is connected with the dorsal nucleus of vagus, which contains parasympathetic fibers of the vagus nerve.

• Activation of the parasympathetic nervous system slows down heart rate.

• To decrease heart rate, stimulate the cardiac inhibitory center.

New Section

This section describes how inhibition of certain centers affects different parts of the body.

Effects on SA Node, AV Node, and Myocardium

• Inhibiting the cardiac accelerator center decreases action potentials moving down sympathetic nerves.

• Decreased action potentials result in reduced release of norepinephrine at SA node, leading to decreased stimulation.

• Similarly, AV node won't receive stimulation from sympathetic fibers if they are inhibited.

• Myocardium also won't receive innervation from the sympathetic nervous system.

• Inhibition of these fibers leads to decreased heart rate and cardiac output.

New Section

This section explains how inhibition of the vasomotor center affects smooth muscle in blood vessels.

Effects on Vasomotor Center and Smooth Muscle

• Inhibiting the vasomotor center decreases action potentials moving down sympathetic nerves.

• Reduced release of norepinephrine results in relaxation of smooth muscle in the tunica media of arterioles.

• Relaxation of smooth muscle leads to an increase in the diameter of blood vessels, known as vasodilation.

New Section

This section discusses the consequences of reduced norepinephrine release on alpha 1 adrenergic receptors.

Effects on Alpha 1 Adrenergic Receptors

• If there is a significant decrease or absence of norepinephrine release, alpha 1 adrenergic receptors are inhibited.

• Inhibition of these receptors prevents constriction of blood vessels.

• The relaxation of smooth muscle in the tunica media causes an increase in the diameter of blood vessels.

New Section

In this section, the speaker discusses the relationship between resistance and radius in blood vessels, and how changes in resistance can affect blood pressure.

Relationship between Resistance and Radius

• Increasing the radius of a blood vessel will significantly decrease its resistance.

• Resistance and radius are inversely proportional.

• Decreasing total peripheral resistance will result in a decrease in blood pressure.

Fixing High Blood Pressure

• Inhibiting the vasomotor nerve center can decrease sympathetic impulses to the tunica media of blood vessels.

• This leads to a decrease in norepinephrine release and relaxation of smooth muscle, causing dilation of blood vessels.

• Dilation increases the diameter and decreases peripheral resistance, resulting in decreased blood pressure.

New Section

In this section, the speaker explains how inhibiting sympathetic fibers can lead to a decrease in epinephrine and norepinephrine release from the adrenal medulla, further reducing blood pressure.

Inhibition of Sympathetic Fibers

• Inhibiting the vasomotor nerve center decreases sympathetic impulses to the tunica media.

• This results in reduced release of epinephrine and norepinephrine from the adrenal medulla.

• Epinephrine binds to alpha-1 adrenergic receptors, contributing to vasoconstriction. Its inhibition leads to vasodilation.

New Section

The speaker introduces the cardiac inhibitory center, which plays a role in regulating heart rate through vagal fibers.

Cardiac Inhibitory Center

• The cardiac inhibitory center is part of the dorsal nucleus of vagus (cranial nerve 10).

• Vagal fibers innervate both SA node (right vagus) and AV node (left vagus).

• Parasympathetic influence from the vagal fibers slows down heart rate.

New Section

The speaker clarifies that there is minimal innervation to the myocardium of the heart, but significant innervation to the SA node, AV node, AV bundle, and Purkinje system.

Innervation of the Heart

• There is no significant innervation to the myocardium (contractile unit) of the heart.

• Vagal fibers primarily innervate the SA node and AV node.

• Left vagus supplies the AV node, while right vagus supplies the SA node.

The transcript provided does not contain enough information for further sections.

New Section

This section discusses the role of the SA node and AV node in the conduction system of the heart, as well as the effect of vagus nerve stimulation on these nodes.

SA Node and AV Node

• The cell in focus could be either an SA node or an AV node, which are part of the conduction system.

• Vagus nerve stimulation releases acetylcholine, which binds to muscarinic type 2 receptors on the SA and AV node membranes.

• Acetylcholine activates G inhibitory protein, which inhibits adenylate cyclase.

• Inhibition of adenylate cyclase decreases cyclic AMP levels, leading to a decrease in protein kinase A levels.

• Decreased protein kinase A activity affects calcium channels on the cell membrane, resulting in decreased calcium entry into the cell.

• G inhibitory protein has three components: alpha inhibitory, beta inhibitory, and gamma inhibitory units.

• Beta and gamma inhibitory units bind to potassium channels on the cell membrane, causing them to open and potassium to leak out.

• Potassium leakage leads to hyperpolarization of the cell and a longer time for action potentials to be sent.

• Decreased heart rate due to hyperpolarization results in decreased cardiac output and blood pressure.

New Section

This section explains how decreasing heart rate through vagus nerve stimulation affects cardiac output and blood pressure.

Heart Rate and Cardiac Output

• Hyperpolarization caused by vagus nerve stimulation leads to a longer time for action potentials to be sent from the heart.

• Longer time between action potentials decreases heart rate.

• Decreased heart rate reduces cardiac output according to the formula: cardiac output = heart rate x stroke volume.

• Decreased cardiac output results in decreased blood pressure.

• Parasympathetic nervous system stimulation, such as through acetylcholine release, has a negative chronotropic action, aiming to decrease heart rate.

• Sympathetic nervous system stimulation has a positive chronotropic action, aiming to increase heart rate and contractility.

• Parasympathetic nervous system does not innervate the myocardium and cannot control contractility.

New Section

This section summarizes the effects of vagus nerve stimulation on heart rate and blood pressure.

Effects of Vagus Nerve Stimulation

• Vagus nerve stimulation decreases heart rate, which may result in bradycardia.

• It also decreases the release of epinephrine and norepinephrine from the adrenal medulla, reducing vasoconstriction response.

• Vasomotor nerve fibers going to the vessels are inhibited, leading to decreased norepinephrine release and vasodilation.

• These effects decrease total peripheral resistance and help lower blood pressure.

• Cardiac accelerator center is inhibited to reduce sympathetic drive to the heart.

New Section

This section mentions that there are further aspects to consider regarding how the body deals with low blood pressure.

Additional Considerations for Low Blood Pressure

• In cases of low blood pressure, JG cells in the kidney are stimulated.

• The correlation between low blood pressure and JG cell stimulation is mentioned but not elaborated upon.

New Section

This section discusses the role of renin in converting angiotensinogen into angiotensin one, and how angiotensin converting enzyme in the lungs converts angiotensin one into angiotensin two.

Renin and Angiotensin Conversion

• Renin cleaves a specific part of angiotensinogen, converting it into angiotensin one.

• Angiotensin converting enzyme in the lungs acts on angiotensin one, converting it into angiotensin two.

New Section

This section explains how stretching of the atria due to high blood pressure leads to the secretion of atrial natriuretic peptide (ANP).

Stretching of Atria and ANP Secretion

• High blood pressure causes stretching of the atria.

• Stretching of the atria activates specialized cells that secrete atrial natriuretic peptide (ANP).

New Section

This section highlights the effects of angiotensin II on various systems in the body.

Effects of Angiotensin II

• Angiotensin II increases thirst and stimulates the release of antidiuretic hormone (ADH).

• It acts on vascular smooth muscle, causing vasoconstriction.

• It stimulates sodium reabsorption in the proximal convoluted tubule, leading to increased blood volume.

• It constricts efferent arterioles and mesangial cells in the kidney.

New Section

This section discusses how the actions of angiotensin II contribute to increased blood pressure.

Angiotensin II and Blood Pressure

• The actions of angiotensin II, such as increasing blood volume and vasoconstriction, lead to increased blood pressure.

• It also affects the efferent arteriole and glomerular mesangial cells in the kidney.

New Section

This section explores the role of atrial natriuretic peptide (ANP) in regulating blood pressure.

Role of ANP in Blood Pressure Regulation

• ANP counteracts the effects of angiotensin II by promoting vasodilation and inhibiting sodium reabsorption.

• It helps reduce blood volume and lower blood pressure.

New Section

This section discusses the effects of angiotensin 2 on blood pressure regulation and the release of aldosterone and ADH.

Effects of Angiotensin 2

• When angiotensin 2 does not bind to its receptor, smooth muscle relaxes, leading to vasodilation and an increase in vessel diameter.

• As vessel diameter increases, total peripheral resistance decreases, resulting in a decrease in blood pressure.

• Angiotensin 2 inhibits the production of aldosterone, which leads to decreased reabsorption of sodium and water.

• Angiotensin 2 also inhibits the release of ADH (antidiuretic hormone) and thirst, reducing water absorption across the GI tract.

Effects on Blood Volume

• Inhibition of aldosterone and ADH release by angiotensin 2 leads to increased urine output (polyuria) and loss of fluid volume.

• Decreased blood volume results in a decrease in end-diastolic volume (EDV), stroke volume, cardiac output, and ultimately blood pressure.

New Section

This section explains how inhibition of aldosterone affects sodium and water reabsorption.

Role of Aldosterone

• Aldosterone is a steroid hormone that stimulates specific genes to produce proteins for sodium channels, potassium channels, and sodium-potassium pumps.

• These proteins facilitate the reabsorption of sodium while promoting potassium excretion.

• Aldosterone also promotes water reabsorption by increasing sodium reabsorption.

Inhibition by Atrial Natriuretic Peptide (ANP)

• Atrial natriuretic peptide inhibits the action of aldosterone by preventing the insertion of sodium channels into the membrane.

• As a result, less sodium is reabsorbed, leading to increased sodium and water loss in the urine.

• This contributes to polyuria (increased urine output) and further decreases blood volume, EDV, stroke volume, cardiac output, and blood pressure.

New Section

This section discusses the inhibitory effects of angiotensin 2 on ADH and its impact on water reabsorption.

Role of ADH

• ADH acts on V2 receptors in the collecting duct to promote the insertion of aquaporin 2 channels into the membrane.

• These channels facilitate water reabsorption by allowing water molecules to move across the cell membrane.

Inhibition by Atrial Natriuretic Peptide (ANP)

• Atrial natriuretic peptide inhibits ADH from acting on its receptors, preventing the insertion of aquaporin 2 channels.

• As a result, water that would have been reabsorbed is lost in the urine.

• This contributes to polyuria (increased urine output), further decreasing blood volume, EDV, stroke volume, cardiac output, and blood pressure.

New Section

This section explains how our body tries to decrease high blood pressure by decreasing heart rate through vagal motor system activation.

Regulation of Heart Rate

• To counter high blood pressure, our body attempts to decrease heart rate.

• The vagal motor system acts on SA node and AV node to decrease cardiac output.

• Decreasing cardiac output helps lower blood pressure.

The transcript provided does not cover all aspects of blood pressure regulation.

New Section

This section discusses the relationship between fluid loss, blood volume, stroke volume, cardiac output, and blood pressure.

Fluid Loss and Blood Volume

• When there is a significant loss of fluid through urine or inadequate water intake due to lack of thirst mechanisms, the blood volume decreases.

• Decreased blood volume leads to a decrease in stroke volume.

• A decrease in stroke volume results in a decrease in cardiac output.

Inhibition of Vasomotor Nerve Center and Cardiac Accel Tory Center

• The vasomotor nerve center is inhibited, leading to the suppression of noradrenaline release.

• The cardiac accel Tory center is also inhibited, which further inhibits the release of epinephrine.

• Inhibition of these centers reduces the release of epinephrine and atrial natriuretic peptide.

Angiotensin 2 Inhibition and Blood Vessel Radius

• Atrial natriuretic peptide inhibits angiotensin 2.

• Inhibiting angiotensin 2 increases the radius of blood vessels by dilating them.

• Increasing the radius of blood vessels decreases resistance, resulting in decreased blood pressure.