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 partially understood. Increased sensitivity to dietary salt intake and to vasoconstrictor 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 days and while they were ingesting a diet containing 250 mEq/day of Na+ for 14 days. During the last 4 days of each dietary regimen, they received 60 mg/day of slow-release nifedipine. Blood pressure response to increasing doses of norepinephrine and angiotensin II was studied at the end of each of the 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 norepinephrine but not to angiotensin II in NIDDM hypertensive subjects. Glomerular filtration rate and renal blood flow were not different during the low and high salt diets. There were no differences in the blood pressure response to norepinephrine or angiotensin II, nor in renal hemodynamic changes among salt-sensitive and salt-resistant NIDDM patients. Nifedipine decreased blood pressure equally in salt-sensitive and salt-resistant hypertensive patients and during the high and the low salt intake. Nifedipine increased renal blood flow, both in salt-sensitive and in salt-resistant individuals, but the differences did not reach statistical significance. Nifedipine decreased the blood pressure response to both norepinephrine and angiotensin II. The studies indicate that an increased reactivity to the pressor action of norepinephrine may contribute to the maintenance of hypertension in NIDDM hypertensive subjects and high salt intake may aggravate the pressor responsiveness to norepinephrine in these patients. Nifedipine is an effective antihypertensive drug in NIDDM patients and its action may be in part related to a decrease in pressor response to norepinephrine and angiotensin II.
Department of Medicine, University of Southern California, Los Angeles, USA. campese@hsc.usc.edu
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D000804:Angiotensin II / Q000494:pharmacology; D000959:Antihypertensive Agents / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology*; D003924:Diabetes Mellitus, Type 2 / Q000150:complications*; D004039:Diet, Sodium-Restricted; D005260:Female; D005919:Glomerular Filtration Rate; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000209:etiology*; D007668:Kidney / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D009543:Nifedipine / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology; D012079:Renal Circulation / Q000502:physiology; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage*
D000959:Antihypertensive Agents; D017673:Sodium Chloride, Dietary; D000804:Angiotensin II; D009543:Nifedipine; D009638:Norepinephrine