Three pathophysiologic mechanisms of primary hypertension.
Three pathophysiologic mechanisms of primary hypertension.
Hypertension is a chronic of blood pressure that, in a long-term causes end-organ damage and results in increased morbidity and mortality. It follows that patient with arterial hypertension may have an increase in cardiac output, an increase in systemic vascular resistance, or both. Three pathophysiologic mechanisms of primary hypertension.
Renin-angiotensin system: The protease renin cleaves angiotensin to yield their inactive peptide angiotensin I. The latter is converted into an active octapeptide, angiotensin II by the angiotension-conversting enzyme (ACE). Though the renin-angiotensin system is widespread in the body, the main source of the renin is the juxtaglomerular apparatus of the kidney. The apparatus senses the renal perfusion pressure and the sodium concentration in the distal tubular fluid. In addition, renin release is stimulated by beta and decreased by alpha adrenoceptor stimulation. Angiotensin II concentration suppress renin secretion via a negative feedbacks loop. Angiotensin II acts on specific angiotensin and receptors causing muscles contraction and the release of aldosterone. The renin-angiotensin-aldosterone system plays an important role in the control arterial pressure including the sodium balance.
Atrial Natriuretic Peptide: is the released from arterial granules. It produces natriuresis, diuresis and a modest decrease in blood pressure, while decreasing plasma renin and aldosterone. Natriuretic peptides also alter synaptic transmission from the osmoreceptors’ is released as a result of the stimulation of atrial stretch receptors. ANP concentration are increased by raised filling pressure and in patients with arterial hypertension and left ventricular hypertrophy as the wall of the left ventricle participates in the secretion of ANP.
Natriuretic peptides play a role in the control of vascular tone and interact with renin-angiotensin-aldosterone system. By inhibiting their degradation, peptidase inhibitors make these naturally occurring peptides more effective, thereby reducing vascular resistance. However, there are only small-scale trials of their efficacy. Overall. recent studies have failed to demonstrate the superiority of modern agents over the more traditional drugs, except in special circumstances. In many patients, effective treatment is achieved by the association of two or more agents with gain in efficacy and reduction of side-effects.
Reference
McCane, K., & Huether, S.(2018). Pathophysiology: The biological basis for disease in adults and children, (8th ed.) St. Louis, MO: Elsevier.
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