학술논문

Decreased blood pressure and vascular smooth muscle tone in mice lacking basolateral [Na.sup.+]-[K.sup.+]-2[Cl.sup.-] cotransporter
Document Type
Academic Journal
Source
The American Journal of Physiology. Nov, 2002, Vol. 283 Issue 5, pH1846, 10 p.
Subject
United States
Language
ISSN
0002-9513
Abstract
The basolateral [Na.sup.+]-[K.sup.+]-2[C1.sup.-] cotransporter (NKCC1) functions in the maintenance of cellular electrolyte and volume homeostasis. NKCC1-deficient ([Nkcc1.sup.-/-]) mice were used to examine its role in cardiac function and in the maintenance of blood pressure and vascular tone. Tail-cuff measurements demonstrated that awake [Nkcc1.sup.-/-] mice had significantly lower systolic blood pressure than wild-type ([Nkcc1.sup.+/+]) mice (114.5 [+ or -] 2.2 and 131.8 [+ or -] 2.5 mmHg, respectively). Serum aldosterone levels were normal, indicating that extracellular fluid-volume homeostasis was not impaired. Studies using pressure transducers in the femoral artery and left ventricle showed that anesthetized [Nkcc1.sup.-/-] mice have decreased mean arterial pressure and left ventricular pressure, whereas myocardial contraction parameters were not significantly different from those of [Nkcc1.sup.+/+] mice. When stimulated with phenylephrine, aortic smooth muscle from [Nkcc1.sup.+/+] and [Nkcc1.sup.-/-] mice exhibited no significant differences in maximum contractility and only moderate doseresponse shifts. In phasic portal vein smooth muscle from [Nkcc1.sup.-/-] mice, however, a sharp reduction in mechanical force was noted. These results indicate that NKCC1 can be important for the maintenance of normal blood pressure and vascular tone. vasculature; hypotension; bumetanide

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