Renal and Cardiovascular Hormonal Regulation of Blood Pressure

Angiotensin II: Systemic and Renal Functions

  • Systemic Vasoconstriction:

    • Angiotensin II acts systemically once it enters the bloodstream and is distributed throughout the body.
    • It functions as a very powerful vasoconstrictor, specifically targeting the smooth muscle of the arterioles.
    • Because the arterial level is the site of the greatest resistance and the greatest decrease in blood pressure (as noted in cardiovascular studies), constricting these vessels leads to a tremendous increase in systemic blood pressure.

  • Impact on the Nephron and Glomerular Filtration Rate (GFR):

    • Angiotensin II acts locally at the arterioles of the glomerulus within the kidney.
    • It specifically constricts the efferent arteriole (the vessel through which filtered blood exits the glomerular capsule).
    • By constricting the exit point (efferent arteriole), it increases the internal pressure within the glomerulus.
    • This mechanism is used to counteract a decrease in GFR; by increasing the pressure within the glomerulus, the Net Filtration Pressure (NFPNFP) is raised, thereby increasing the GFR.

The Adrenal Gland and Aldosterone

  • Source and Context:

    • Aldosterone is secreted by the adrenal glands, specifically from the cortex.
    • The adrenal cortex is divided into three distinct areas/zones.

  • Mechanism of Action:

    • Aldosterone is released into the blood and travels to the nephron in the kidney.
    • Its primary function is to increase sodium retention, which refers to increasing the reabsorption of sodium out of the filtrate and back into the blood.
    • The Physical Principle: "Wherever sodium moves, water moves." Because sodium is reabsorbed, water follows it automatically through osmosis.

  • Effect on Blood Volume and Pressure:

    • A decrease in blood volume and a corresponding decrease in blood pressure serve as the triggers for aldosterone release.
    • As water is reabsorbed into the peritubular capillaries, it immediately re-enters the cardiovascular system.
    • This increases the total blood volume, which is described as the fastest way the body can increase blood pressure.

Antidiuretic Hormone (ADH)

  • Synthesis and Storage:

    • The hypothalamus synthesizes two primary hormones: ADH and Oxytocin.
    • These hormones are transported via axons and stored in the posterior pituitary gland until release.

  • Function and Diuresis:

    • Diuresis is defined as the loss of water in the urine, resulting in watery urine.
    • Antidiuretic Hormone (ADH) acts against this process to stop water loss.
    • Angiotensin II stimulates the production and release of ADH.

  • Renal Impact:

    • ADH stimulates the reabsorption of water directly from the filtrate in the renal tubules.
    • This water is reabsorbed by the peritubular capillaries and returned to the cardiovascular system.
    • The result is an increase in blood volume and a subsequent increase in blood pressure.

Central Nervous System and Sympathetic Activation

  • CNS Stimulation:

    • Angiotensin II affects the central nervous system by stimulating the thirst centers located in the brain.
    • This stimulation leads to an increase in fluid intake, which increases blood volume and brings blood pressure up.

  • Sympathetic Tone:

    • Angiotensin II increases sympathetic tone, which refers to increased sympathetic nervous system stimulation.
    • This affects both the kidneys and the cardiovascular system.

  • Cardiac Effects:

    • Heart Rate: Sympathetic stimulation acts on the SA node to increase the heart rate (beats per minute).
    • Contractility: It increases the force of contraction in the cardiac muscle of the ventricles.
    • Cardiac Output: By increasing both heart rate and contractility, the total cardiac output is increased, which directly raises blood pressure.

Atrial and Brain Natriuretic Peptides (ANP and BNP)

  • Endocrine Function of the Heart:

    • The heart functions as an endocrine organ when blood volume becomes excessively high.
    • ANP (Atrial Natriuretic Peptide): Produced by the atria.
    • BNP (B-type Natriuretic Peptide): Produced by the ventricles.

  • Trigger for Release:

    • These hormones are triggered by the overfilling of the heart chambers, which causes the overstretching of the cardiac muscle.

  • Mechanism at the Nephron:

    • ANP and BNP cause the dilation of afferent arterioles (increasing blood flow into the glomerulus) and the constriction of efferent arterioles (backing up pressure).
    • This combination significantly increases the Net Filtration Pressure (NFPNFP).

  • Physiological Result:

    • The increased NFPNFP pushes more water out of the blood and into the tubular system.
    • The resulting urine has a high concentration of water.
    • This allows the body to "pee out" the excess volume, bringing blood volume and pressure back down to normal levels.

General Principles of Blood Volume and GFR

  • Flowchart Logic:
    • If blood volume rises, the filtration pressure at the glomerulus increases automatically.
    • Standard Net Filtration Pressure (NFPNFP) is approximately 10 mmHg10\,mmHg.
    • If NFPNFP increases (e.g., to 15 mmHg15\,mmHg), more liquid (plasma) is pushed out of the capillaries into the filtrate.
    • If the volume is too high, the urine will contain more water to reduce blood volume and pressure.

Questions & Discussion

  • Question: How does sympathetic stimulation increase cardiac output?
  • Response: At the level of the SA node, it increases the heart rate, resulting in more beats per minute. This impacts cardiac output.
  • Question: Any place else that sympathetic stimulation might influence cardiac output?
  • Response: It causes increased contraction of the cardiac muscle. If contractility in the ventricles is increased, it helps raise blood pressure through the Frank-Starling law (relating to ventricular stretching and force of contraction).