The Plasma Renin Test Reveals the Contribution of Body Sodium-Volume Content (V) and Renin-Angiotensin (R) Vasoconstriction to Long-Term Blood Pressure

Abstract

Body sodium works together with the plasma renin-angiotensin system to ensure adequate blood flow to the tissues. Body sodium content determines the extracellular fluid (ECF) volume ensuring that, with each heart beat, a sufficient volume of fluid is delivered into the arterial space. At the same time the kidneys monitor ECF volume and blood pressure (BP), so that the juxtaglomerular cells can adjust their net secretion rate of renin to maintain an appropriate plasma renin activity (PRA) level. Plasma renin produces angiotensin II (Ang II) to constrict the arterioles and thereby ensure sufficient BP to deliver an appropriate rate of flow for cardiovascular homeostasis. The low renin, sodium-volume dependent (V) form of essential hypertension occurs whenever body sodium content increases beyond the point where plasma renin-angiotensin vasoconstrictor activity is turned off. In contrast, medium to high renin (R) hypertension occurs when too much renin is secreted relative to the body sodium content. Thus, BP = V × R. This volume-vasoconstriction dual support of long-term hypertension is validated by the fact that all effective long-term antihypertensive drug types are either (i) natriuretic to reduce body salt and volume content (anti-V), or (ii) antirenin to reduce or block the activity of the circulating renin-angiotensin system (anti-R). The PRA test defines the relative participation of the concurrent volume and vasoconstrictor factors. In the hypertensive patient PRA testing can guide initiation, addition or subtraction of anti-V or anti-R antihypertensive drug types to thereby improve BP control and prognosis while reducing drug type usage and cost.

Hypertension

“…60 The former occurs whenever body sodium content increases beyond the point where plasma RAAS activity is turned off, whereas the latter occurs when too much renin is secreted relative to the body sodium content. Antihypertensive treatment should then be aimed at reducing either body salt and volume content (diuretics, calcium antagonists) or RAAS activity (RAAS blockers and β-adrenergic antagonists; the latter suppress renin release).…”

Heterogeneity in Early Responses in ALLHAT (Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial)

“…4 Biologically, patients with high plasma renin activity have vasoconstrictiondependent hypertension that may respond better to reninangiotensin-aldosterone system inhibitors, whereas people with low plasma renin activity may have volume-dependent hypertension that is more responsive to diuretics. 31 Pressor responses have been described in people with low plasma (Table S5). CHD indicates coronary heart disease; CVD, cardiovascular disease; and MI, myocardial infarction.…”

The balance between human maternal plasma angiotensin II and angiotensin 1-7 levels in early gestation pregnancy is influenced by fetal sex

“…[1][2][3] A significant increase in plasma volume is essential for a successful pregnancy; these changes in plasma volume are mediated in part by the actions of angiotensin (Ang) II on the adrenal cortex, which releases aldosterone and stimulates fluid retention. 4 Ang II has vasopressor effects, increasing systemic vascular resistance through central and peripheral actions. The RAAS is activated in early pregnancy to maintain blood pressure as maternal peripheral blood flow increases, particularly in the skin, 5 kidneys 6 and uterus.…”