Hypotension activates renal baroreceptors, which results in the secretion of renin and consequent activation of the renin-angiotensin-aldosterone system (RAAS).
Hypovolemia results in hypoperfusion of kidneys, activation of renal baroreceptors, and secretion of renin, which activates the renin-angiotensin-aldosterone system.
Decreased NaCl delivery to the macula densa cells located in the distal tubule of the nephron results in the activation of the renin-angiotensin-aldosterone-system.
Sympathetic outflow stimulating B1-receptors results in the secretion of renin and activation of the renin-angiotensin-aldosterone-system.
Angiotensin II is the key mediator of the renin-angiotensin-aldosterone system. It is synthesized in the pulmonary capillary endothelium. Angiotensin II promotes vasoconstriction and secretion of aldosterone, and antidiuretic hormone. It also activates Na reabsorption in the proximal convoluted tubule.
Aldosterone is a part of the renin-angiotensin-aldosterone system. It is a steroid hormone that affects water and salt regulation in the body. It increases Na and water reabsorption in the kidneys.
Angiotensin II stimulates the release of antidiuretic hormone, which promotes the insertion of aquaporins in the collecting duct and induces reabsorption of the free water.
Atrial natriuretic peptide (ANP) is released in response to the distension of the atria of the heart (e.g., volume overload) while brain natriuretic peptide (BNP) is released in response to ventricular distension. These hormones increase renal sodium excretion (natriuresis) and inhibit renin secretion. Thus, they effectively suppress RAAS.
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