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Exaggerated renal vasodilator response to calcium entry blockade in first-degree relatives of essential hypertensive
Insights
Individuals with a family history of hypertension show altered renal vascular responses to diltiazem, suggesting potential inherited factors influencing blood pressure regulation.
Area of Science:
- Nephrology
- Cardiovascular Physiology
- Hypertension Research
Background:
- Essential hypertension may have an inherited renal component.
- Understanding renal vascular tone determinants is crucial for hypertension research.
Purpose of the Study:
- To investigate the determinants of renal vascular tone in normotensive individuals.
- To assess the influence of sodium intake and family history of hypertension on renal vascular responses.
- To explore the role of angiotensin in modulating renal vascular tone.
Main Methods:
- Infusion of diltiazem or acetylcholine into the renal artery in 52 normotensive subjects.
- Measurement of renal blood flow using 133Xe.
- Subjects were studied under restricted (10-mEq) and normal (200-mEq) sodium intake.
Main Results:
- Restricted sodium intake potentiated diltiazem's renal vascular effects, indicating angiotensin's role.
- Angiotensin II enhanced diltiazem's renal vasodilator action in subjects without hypertension history.
- Subjects with a family history of hypertension exhibited an enhanced renal vascular response to diltiazem.
Conclusions:
- Renal vascular responses to diltiazem are influenced by sodium intake and family history of hypertension.
- The enhanced response to diltiazem in subjects with a family history suggests an underlying abnormality in renal vascular tone control.
- Acetylcholine responses were not affected by sodium intake or family history, highlighting diltiazem's specificity.
Abstract:
Because an inherited renal factor may contribute to essential hypertension in humans, the study of family members is attractive. To assess the determinants of renal vascular tone, graded doses of either diltiazem (10-1000 micrograms/min) or acetylcholine (1-100 micrograms/min) were infused into the renal artery in 52 normotensive subjects, 16 with and 36 without a family history of hypertension when they were in balance on either a 10-mEq or 200-mEq sodium intake. Renal blood flow was measured with 133Xe. Restricted sodium intake potentiated renal vascular responses to diltiazem (p less than 0.01), suggesting a role for angiotensin as a determinant. In four subjects with no family history of hypertension on a 200-mEq sodium intake, angiotensin II in subpressor doses (1 ng/kg/min i.v.) induced renal vasoconstriction and enhanced the renal vasodilator action of diltiazem (p less than 0.001). In subjects with a family history of hypertension, the renal vascular response to diltiazem was enhanced (p less than 0.01) despite similar values of plasma renin activity, angiotensin II concentration, and sodium excretion. Because responses to acetylcholine were modified neither by sodium intake nor by family history, specificity for diltiazem was suggested. The intriguing possibility is raised that the enhanced renal vascular response to diltiazem reflects an abnormality in the control of renal vascular tone in the offspring of essential hypertensive subjects.