This map shows the link between the mechanisms of hypertension and how antihypertensive agents work. Blood pressure is a product of cardiac output and total peripheral vascular resistance, so the increase in one or both of these factors leads to hypertension. Blood pressure is controlled by neural and humoral systems which include:
- Renin-Angiotensin Aldosterone System,
- Increased sympathetic discharge,
- Increased sodium and chloride concentrations in extracellular fluid volume, and
- Vasodilators deficiency
This part of the map explains each of hypertension contributing factors including the inter-related links between them. Antihypertensive agents are stated around the pathophysiology part to illustrate the effect or the site of action of each agent on the pathophysiology using dotted lines. Hypertension pathophysiology part of the map starts with Renin-Angiotensin System (RAS) which ends with the production of angiotensin II which is a vasoconstrictor that stimulates the autonomic centers in the brain resulting in increased sympathetic discharge. It also stimulates aldosterone and antidiuretic hormone. Antidiuretic hormone is also stimulated by increased sodium and chloride concentration in the extracellular fluid, causing sodium and water retention and an increase in peripheral vascular resistance. The increase in the sympathetic discharge increases heart rate and contractility, so increasing cardiac output. Norepinephrine causes vasoconstriction and induces kidney sodium retention resulting in an increase in peripheral vascular resistance. Another factor for the development of hypertension is the deficiency in the synthesis of vasodilators as nitric oxide and prostacyclin and the degradation of bradykinin which is also a vasodilator, in the face of the normal release of endothelin and the increased release of Angiotensin I and Angiotensin II which are vasoconstrictors.
Pharmacological treatment of hypertension
It includes the following agents: ACE inhibitors’ mechanism of action includes inhibiting Angiotensin-Converting Enzyme (ACE), blocking the degradation of bradykinin, and stimulating the synthesis of some vasodilators, so decreasing tissue peripheral resistance. Angiotensin II Receptor Blockers (ARB) block angiotensin 2 receptors. The mechanism of action of diuretics includes decreasing plasma and stroke volume and so decreasing blood volume which in turn decreases cardiac output. Thiazide diuretics also decrease peripheral vascular resistance by mobilizing Na & water from arteriolar walls and by acting as direct vasodilators on blood vessels. Aldosterone antagonists are potassium-sparing diuretics that competitively bind to aldosterone receptors and so decrease both cardiac output and peripheral vascular resistance. Direct vasodilators work directly on blood vessels. Dihydropyridine calcium channel blockers block voltage-gated calcium channels (VGCC) in blood vessels causing vasodilatation. While, nondihydropyridine calcium channel blockers block voltage-gated calcium channels (VGCC) in cardiac muscles, so they act as negative chronotropic, negative dromotropic, and negative inotropic agents and cause a decrease in cardiac output. Sympathetic depressants act on different sites to decrease sympathetic discharge. Among the commonly used sympathetic depressants are beta-blockers. Beta-blockers also inhibit renin release so decrease tissue peripheral resistance in addition to their negative inotropic and negative chronotropic effects that decrease cardiac output. This was an explanation for hypertension pathophysiology linked by mechanisms of action of antihypertensive agents and effects on cardiac output and/or peripheral vascular resistance and consequently blood pressure.
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