Arteriolar Lumen Diameter Research Articles

Contribution of tubuloglomerular feedback to renal arteriolar angiotensin II responsiveness

The purpose of the present study was to test the hypothesis that a component of the afferent arteriolar vasoconstrictor response to angiotensin II (Ang II) requires an intact tubuloglomerular feedback (TGF) mechanism. Enalaprilat-treated male Sprague-Dawley rats served as tissue donors for study of renal microvascular function using the in vitro blood-perfused juxtamedullary nephron technique. Arteriolar lumen diameter responses to exogenous Ang II were determined before and after TGF blockade (papillectomy or 50 microM furosemide). Before TGF blockage, 10 nM Ang II significantly reduced diameters of both mid-afferent (53 +/- 5%) and efferent (43 +/- 9%) arterioles. TGF blockade did not alter baseline diameter of either arteriole, but significantly blunted the mid-afferent vasoconstriction evoked by 10 nM Ang II (44 +/- 7% inhibition by papillectomy; 43 +/- 10% inhibition by furosemide). Similar behavior was observed at afferent arteriolar sites near the glomerulus; however, efferent arteriolar Ang II responsiveness was not altered by papillectomy. The impact of TGF blockade on afferent arteriolar Ang II responsiveness was most prominent at high peptide concentrations (10 nM), while not significantly influencing the response to 1 nM Ang II. In contrast, the afferent vasoconstrictor effect of norepinephrine was unaffected by papillectomy. These data indicate that the vasoconstrictor influence of exogenous Ang II on afferent, but not efferent, arterioles of intact juxtamedullary nephrons includes both TGF-dependent and TGF-independent components.

Arteriolar vasoconstriction in rat cremaster muscle induced by local heat stress.

The effect of moderate local heat stress on arteriolar tone in the cremaster muscle of anesthetized rats was investigated by direct microscopic observation. Muscle temperature was raised from the in vivo temperature of 34.5 to 38 degrees C, over a 5-min period, by elevating bath temperature. Muscle temperature, arteriolar lumen diameter, and arteriolar red blood cell velocity were continuously recorded. A number of the smallest arterioles studied (approximately 30 micrometers lumen diam) underwent a rapid and significant vasoconstriction near 36 degrees C. Denervation of the muscle eliminated the constrictor response. Addition of an alpha-blocking agent (dibenzyline to the denervated muscle unmasked the constriction, but the percent of arterioles demonstrating thermal reactivity remained decreased. We conclude that in some skeletal muscle beds a local thermoregulatory mechanism may exist whereby blood is shunted away from the tissue during heat stress at rest.