Endocrinal or hormonal intervention in the cardiovascular system is predominantly exerted by the catecholamines – epinephrine and norepinephrine, as well as a slew of hormones that interact with renal function to modulate blood volume.
Epinephrine and Norepinephrine
The adrenal medulla releases epinephrine and norepinephrine, catecholamines that enhance and extend the sympathetic or "fight or flight" physiological response. These hormones escalate heart rate and the force of contraction while temporarily inducing vasoconstriction in organ systems not essential for the flight or fight response. Concurrently, they redirect blood flow toward the liver, muscles, and heart.
Antidiuretic Hormone
Antidiuretic hormone (ADH), also termed vasopressin, is synthesized by cells in the hypothalamus and transported through the hypothalamic-hypophyseal tract to the posterior pituitary, where it remains stored until released upon neural stimulation. The primary stimulus prompting the hypothalamus to release ADH is an increase in tissue fluid osmolarity, usually in response to a substantial loss of blood volume. ADH sends signals to its target cells in the kidneys to reabsorb more water, thereby minimizing additional fluid loss via urine. This action elevates overall fluid levels, aiding in the restoration of blood volume and pressure. Additionally, ADH induces peripheral vasoconstriction.
Renin-Angiotensin-Aldosterone Mechanism
The renin-angiotensin-aldosterone mechanism exerts a significant impact on the cardiovascular system. The release of the enzyme renin by juxtaglomerular (JG) cells in the kidneys in response to decreased blood pressure kickstarts this mechanism. Renin transforms angiotensinogen, a plasma protein synthesized by the liver, into angiotensin-I. Angiotensin-I is then converted into angiotensin II in the lungs, a reaction catalyzed by the enzyme angiotensin-converting enzyme (ACE).
Angiotensin II, a potent vasoconstrictor, substantially raises blood pressure and also induces the release of ADH and aldosterone. Aldosterone promotes the kidneys' reabsorption of sodium into the blood. Since water tends to follow sodium, this action increases the reabsorption of water, which subsequently raises blood volume and pressure. Angiotensin-II also stimulates the thirst center in the hypothalamus, thereby promoting fluid consumption further increasing blood volume and pressure.
Erythropoietin
Erythropoietin (EPO) is secreted by the kidneys in response to decreased blood flow or oxygen levels. EPO triggers the production of erythrocytes within the bone marrow. Erythrocytes, the primary formed element of blood, may contribute to 40 percent or more of blood volume, significantly influencing viscosity, resistance, pressure, and flow. Furthermore, EPO functions as a vasoconstrictor. Oversynthesis of EPO or excessive intake of synthetic EPO, particularly to enhance athletic performance, can escalate viscosity, resistance, and pressure and decrease flow in addition to EPO's role as a vasoconstrictor.
Atrial Natriuretic Hormone
Atrial natriuretic hormone (ANH), secreted by cells in the heart's atria, is released when blood volume is sufficiently high to cause extreme stretching of the cardiac cells. Ventricular cells produce a similar hormone, termed B-type natriuretic hormone. Natriuretic hormones act antagonistically to angiotensin II, promoting the excretion of sodium and water from the kidneys and suppressing the production and release of renin, aldosterone, and ADH. These actions collectively promote fluid loss from the body, leading to a reduction in both blood volume and blood pressure.
