Dietary salt intake, blood pressure and the kidney in hypertensive patients with non-insulin dependent diabetes mellitus

The mechanisms responsible for hypertension in NIDDM patients are only part ially understood. Increased sensitivity to dietary salt intake and to vasoc onstrictor hormones are among the mechanisms proposed. We have studied 19 hypertensive NIDDM patients 7 salt-sensitive and 12 salt -resistant while they were ingesting a diet with 20 mEq/day of Na+ for 9 da ys and while they were ingesting a diet containing 250 mEq/day of Na+ for 1 4 days. During the last 4 days of each dietary regimen, they received 60 mg /day of slow-release nifedipine. Blood pressure response to increasing dose s of norepinephrine and angiotensin II was studied at the end of each of th e four phases of the study. High salt intake increased blood pressure and decreased heart rate in these patients. High salt intake also increased the vascular response to norepin ephrine but not to angiotensin II in NIDDM hypertensive subjects. Glomerula r filtration rate and renal blood flow were not different during the low an d high salt diets. There were no differences in the blood pressure response to norepinephrine or angiotensin II, nor in renal hemodynamic changes amon g salt-sensitive and salt-resistant NIDDM patients. Nifedipine decreased bl ood pressure equally in salt-sensitive and salt-resistant hypertensive pati ents and during the high and the low salt intake. Nifedipine increased rena l blood flow, both in salt-sensitive and in salt-resistant individuals, but the differences did not reach statistical significance. Nifedipine decreas ed the blood pressure response to both norepinephrine and angiotensin II. The studies indicate that an increased reactivity to the presser action of norepinephrine may contribute to the maintenance of hypertension in NIDDM h ypertensive subjects and high salt intake may aggravate the presser respons iveness to norepinephrine in these patients. Nifedipine is an effective ant ihypertensive drug in NIDDM patients and its action may be in part related to a decrease in presser response to norepinephrine and angiotensin II.