title: 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.
authors.affiliation: Department of Cardiothoracic Surgery, Weill Cornell Medical College, New York, New York, USA.
authors.forename: John H
authors.initials: JH
authors.lastname: Laragh
authors.forename: Jean E
authors.initials: JE
authors.lastname: Sealey
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000809:Angiotensins / Q000502:physiology*; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology*; D001794:Blood Pressure / Q000187:drug effects*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D004232:Diuretics / Q000494:pharmacology; D045604:Extracellular Fluid / Q000502:physiology*; D006801:Humans; D006973:Hypertension / Q000503:physiopathology; D000451:Mineralocorticoid Receptor Antagonists; D008955:Models, Cardiovascular; D012083:Renin / Q000097:blood* / Q000378:metabolism; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000502:physiology*; D012964:Sodium / Q000037:antagonists & inhibitors / Q000502:physiology*; D014661:Vasoconstriction / Q000187:drug effects; D000092502:Renin Inhibitors
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000809:Angiotensins; D000959:Antihypertensive Agents; D002121:Calcium Channel Blockers; D004232:Diuretics; D000451:Mineralocorticoid Receptor Antagonists; D012083:Renin; D012964:Sodium; D000092502:Renin Inhibitors