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Published on: June 10, 2015
Chlorthalidone reduces vascular hyperresponsiveness in DOCA-salt hypertensive rats
A M Cabral1, M N Musso, N S Bissoli
1Dept. Physiological Sciences, UFES, Brazil.
Summary
Long-term chlorthalidone treatment lowers blood pressure by reducing blood vessel responsiveness to neurohormones. This diuretic effect is linked to decreased sodium levels and vascular hyperresponsiveness.
Area of Science:
- Pharmacology
- Cardiovascular Physiology
- Nephrology
Background:
- The precise mechanisms underlying the antihypertensive effects of diuretics are not fully understood.
- Diuretics are commonly prescribed for hypertension, necessitating research into their vascular actions.
Purpose of the Study:
- To investigate if long-term chlorthalidone administration reduces the responsiveness of resistance blood vessels to neurohormones.
- To elucidate the role of vascular reactivity in the antihypertensive action of chlorthalidone.
Main Methods:
- Experiments were conducted on deoxycorticosterone acetate (DOCA)-salt hypertensive rats, with and without chlorthalidone treatment.
- Mean arterial pressure was measured in freely moving rats, and responses of isolated perfused mesenteric arteries to norepinephrine, serotonin, and vasopressin were assessed.
Main Results:
- Chlorthalidone treatment significantly lowered resting mean arterial pressure in DOCA-salt rats.
- Vascular hyperresponsiveness to norepinephrine, serotonin, and vasopressin was observed in DOCA-salt rats but attenuated by chlorthalidone.
- Chlorthalidone normalized elevated plasma sodium levels in DOCA-salt hypertensive rats.
Conclusions:
- Long-term chlorthalidone treatment decreases vascular hyperresponsiveness to key neurohormones.
- Reduced vascular hyperresponsiveness, coupled with decreased extracellular sodium, may represent a significant mechanism for the antihypertensive effects of chlorthalidone.
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