Fisiología Renal - Control de la Filtración glomerular y flujo sanguíneo (IG:@doctor.paiva)

Control of Glomerular Filtration and Renal Blood Flow

Introduction to Renal Physiology

• The class introduces the topic of renal physiology, focusing on glomerular filtration control and renal blood flow.

• Key concepts include hormonal control, tubuloglomerular feedback, and autoregulation.

Determinants of Glomerular Filtration

• Glomerular filtration is determined by net filtration pressure (NFP) and the glomerular coefficient.

• NFP is calculated from hydrostatic pressures in the glomerulus and Bowman’s capsule, with values being 60 mmHg for glomerular capillary pressure and 18 mmHg for Bowman’s capsule pressure.

Calculation of Net Filtration Pressure

• The net filtration pressure is derived as follows: NFP = (60 - 18 - 32), resulting in an NFP of 10 mmHg.

• The glomerular filtration rate (GFR) can be expressed as GFR = Kf × NFP, where Kf is the glomerular coefficient.

Factors Influencing Glomerular Filtration Rate

• Sympathetic nervous system activation has varying effects; mild stimulation has little impact while intense stimulation during severe hemorrhage significantly reduces both blood flow and GFR.

• Hormones like norepinephrine and epinephrine cause vasoconstriction in renal arterioles, reducing blood flow and GFR under extreme conditions.

Role of Endothelin in Vasoconstriction

• Endothelin is released due to endothelial damage, acting as a potent vasoconstrictor that decreases renal blood flow and GFR.

Angiotensin II's Functionality

• Angiotensin II primarily constricts the efferent arterioles, increasing glomerular pressure to maintain GFR during hypotensive states or volume loss.

• It counteracts reductions in GFR by enhancing hydrostatic pressure within the glomeruli through its action on efferent arterioles.

Understanding Glomerular Filtration and Regulation

Mechanisms of Vasoconstriction and Filtration

• The front generates a false constriction primarily at the afferent arteriole, as it is protected by opposing substances that regulate pressure, thus affecting arterial constriction.

• Increased hydrostatic pressure in the capillaries leads to enhanced glomerular filtration; however, reduced flow to peritubular capillaries results in increased reabsorption of water and sodium due to lower flow rates.

• The release of renin is stimulated by volume loss or low sodium diets, which helps maintain glomerular filtration through tubuloglomerular feedback mechanisms.

Role of Angiotensin II

• Angiotensin II plays a crucial role in maintaining stable glomerular filtration despite fluctuations in blood pressure or volume loss.

• Nitric oxide and prostaglandins positively influence glomerular capillary flow by dilating vessels, while certain genes can inhibit prostaglandin effects.

Tubuloglomerular Feedback Mechanism

• The nephron's structure includes the glomerulus and afferent/efferent arterioles; tubuloglomerular feedback involves specialized cells (macula densa) that monitor sodium concentration.

• This feedback mechanism relies on the juxtaglomerular apparatus formed by macula densa cells and juxtaglomerular cells located in arterial walls.

Response to Decreased Blood Pressure

• A drop in blood pressure reduces glomerular filtration rate (GFR), leading to slower blood flow into the nephron, which increases sodium reabsorption due to decreased tubular concentrations.

• Lower sodium concentrations detected by macula densa trigger two responses: direct reduction of resistance at the afferent arteriole and stimulation of renin release from juxtaglomerular cells.

Renin-Angiotensin System Activation

• Renin activates angiotensinogen from the liver into angiotensin I, which converts into angiotensin II via ACE (Angiotensin-Converting Enzyme).

Understanding Autoregulation of Glomerular Filtration

Mechanisms of Autoregulation in the Kidneys

• The decrease in sodium chloride in the macula densa directly triggers vasodilation, which helps maintain glomerular filtration rate (GFR).

• An increase in pressure within the arterioles causes vascular wall stretching, enhancing calcium permeability and leading to smooth muscle contraction (vasoconstriction).

• This autoregulatory mechanism is crucial for protecting kidney function during sudden increases in blood pressure by preventing damage to capillaries.

• Significant fluctuations in blood pressure (e.g., drops to 70 mmHg or spikes to 180 mmHg) only affect GFR by about 10%, thanks to autoregulation.