Activation of Na+, H+ exchanger produces vasoconstriction of renal resistance vessels.

Content Provider	Semantic Scholar
Author	Tepel, Martin Jankowski, Joachim Ruess, Christian Steinmetz, Martin Giet, Markus Van Der Zidek, Walter
Copyright Year	1998
Abstract	To evaluate the influence of the sodium/proton exchanger (Na+,H+ exchanger) on the constriction of rat resistance vessels and on the iliac artery, the isometric vasoconstrictions of renal resistance vessels and strips from iliac artery derived from Wistar-Kyoto rats were measured using a vessel myograph. The Na+,H+ exchanger was activated by intracellular acidification using propionic acid. Cytosolic pH (pHi) and cytosolic free sodium concentration ([Na+]i) in vascular smooth muscle cells were measured using the fluorescent dye technique. The activation of the Na+,H+ exchanger increased the [Na+]i by 12.4 +/- 1.3 mmol/L (n = 8). The activation of the Na+,H+ exchanger caused a contractile response of the renal resistance vessels (increase of tension, 1.5 +/- 0.1 x 10(-3) N; n = 13) and of the rat iliac artery (increase of tension, 7.5 +/- 0.8 x 10(-3) N; n = 5). The contractile response after activation of the Na+,H+ exchanger was significantly inhibited in the absence of external sodium or in the presence of amiloride, confirming the involvement of the Na+,H+ exchanger. The contractile response after activation of the Na+,H+ exchanger was significantly reduced in the absence of external calcium, after inhibition of calcium channels by nifedipine, and in the presence of an intracellular calcium antagonist 8-(diethylamino-)-octyl-3,4,5-trimethoxybenzoate (TMB-8), indicating that the activation of the Na+,H+ exchanger consecutively caused transplasma membrane calcium influx. On the other hand, the inhibition of the Na+,Ca2+ exchanger by NiCl2 significantly increased the vasoconstriction of renal resistance vessels after activation of the Na+,H+ exchanger. The activation of the Na+,H+ exchanger produces vasoconstriction by an increased cytosolic sodium concentration, inhibition of the Na+,Ca2+ exchanger, and activation of transplasma membrane calcium influx through potential dependent calcium channels.
Starting Page	86
Ending Page	87
Page Count	2
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PubMed reference number	9799038v1
Volume Number	11
Issue Number	10
Journal	American journal of hypertension
Language	English
Access Restriction	Open
Subject Keyword	Amiloride Blood Vessel Tissue Bone structure of ilium Calcium Channel Blockers Fluorescent Dyes Muscle Cells Muscle, Smooth, Vascular Myocytes, Smooth Muscle Nifedipine Propionic acid Protons Smooth muscle (tissue) Sodium Structure of iliac artery TMB 8 Tension Tissue membrane Vascular constriction (function)
Content Type	Text
Resource Type	Article