Endothelial Ca2+ in afferent arterioles during myogenic activity

We measured endothelial Ca2+ concentration ([Ca2+]) in juxtamedullary afferent arterioles in response to step changes in perfusion pressure. Measurements were made with fura 2 using a fluorescence-imaging system designed to measure Ca2+ in whole tissues and minimize potentially harmful effects of ultraviolet illumination. The system yielded the typical sigmoidal relationship between fluorescence-emission ratio and [Ca2+] in vitro and was sensitive to endothelial Ca2+ transients elicited by bradykinin. Our goal was to determine whether changes in endothelial Ca2+ trigger events that cause myogenic vasoconstriction. Bradykinin, acting via endothelial cells, and sodium nitroprusside (SNP), acting independently, triggered vasodilation; bradykinin but not SNP increased endothelial Ca2+. Increased perfusion pressure caused vasoconstriction and a modest rise in endothelial Ca2+. Because the rise in Ca2+ with bradykinin initiates the vasodilation, the small rise in Ca2+ with pressure cannot cause vasoconstriction. Our results suggest that myogenic constriction is triggered from within vascular smooth muscle cells and that some other phenomenon, most likely increased shear stress, increases endothelial Ca2+ and modulates the myogenic reaction.

Vasoconstrictor effect of angiotensin and vasopressin in isolated rabbit afferent arterioles

The present studies were performed to examine the vasoconstrictor effect of angiotensin II (ANG II), angiotensin III (ANG III), and vasopressin in isolated afferent arterioles of the rabbit kidney. Afferent arterioles were dissected together with their glomerulus and perfused with a pressure head of 120 cmH2O. Changes in vasomotor tone were assessed as diameter changes on videotaped recordings. Afferent arterioles responded to the angiotensins and vasopressin with dose-dependent reductions in vascular diameters with half-maximum responses being observed at concentrations between 10(-9) and 10(-8) M. Responses to ANG II and III were inhibited by saralasin. Contractile responses to ANG II and vasopressin were not altered by prior occlusion of the efferent arteriole, suggesting that afferent vasoconstriction does not represent a myogenic reaction to an increase in efferent resistance. The vasoconstrictor response to ANG II was largely eliminated by removal of the glomerulus and the distal-most portion of the afferent arteriole, whereas the response to vasopressin remained intact. Our data are consistent with the notion that the juxtaglomerular apparatus (JGA) and/or glomerulus may control proximal afferent arteriolar contractility by electrotonic or myogenic coupling mechanisms or by producing cofactors that modulate vasomotor responses.

Carotid Artery Vasospasm Complicating Extensive Skull Base Surgery: Cause, Prevention, and Management

Arterial spasm is rarely encountered in the uncomplicated cervical lymphadenectomy. Intense, often dramatic, vasospasm of the internal carotid artery, however, is not infrequently observed in the removal of skull-base lesions. This myogenic reaction is independent of autonomic innervation, occurs more frequently in younger patients, and appears to be due mainly to longitudinal arterial traction and prolonged arterial contact with fresh blood. A case of severe internal carotid artery spasm, which led to a fatal stroke in a young woman who underwent removal of a large glomus jugulare tumor, is presented to emphasize not only the lethal potential of carotid spasm, but intraoperative changes in the character of the artery which suggest the need for immediate spasmolysis. Perioperative guidelines for the prevention and treatment of arterial spasm—including topical and systemic pharmacotherapy and refined surgical techniques—are outlined on the basis of our subsequent experience.

Nonuniformity of CBF response to NE- or ANG II-induced hypertension in rabbits

The regional response of brain vasculature to moderate hypertension was investigated using two hypertensive drugs, norepinephrine (NE) and angiotensin II (ANG II), infused intravenously at low concentrations (increase in blood pressure 15–40 mm Hg). Regional cerebral blood flow (rCBF) was measured in unanesthetized and anesthetized rabbits using the [14C]ethanol saturation technique. In both groups of animals, NE and ANG II induced regional differences in the flow changes as compared with controls, confirming a regional (or segmental) heterogeneity in the regulatory mechanisms to hypertension. The responses to identical rises in blood pressure (BP) in most of the structures analyzed depended on the drug used. In the unanesthetized rabbits, the increase in vascular resistance induced by NE was greater than that induced by ANG II. With the two drugs, there was no correlation between the flow changes in any of the structures considered and either the BP increase or the BP level in unanesthetized animals. However, these flow changes were correlated with the BP increase in anesthetized animals, although differences between the effects of NE and ANG II were again observed. This study suggests that cerebrovascular regulatory mechanisms in hypertension are probably more complex than a simple myogenic reaction. Their heterogeneity and their dependence both on the cause of hypertension and on the presence of anesthetics suggest the intervention of an integrating pathway.

Microvascular myogenic reaction in the wing of the intact unanesthetized bat

Microvascular dimension and flow responses to stepwise changes in arterial and venous pressures, ranging from zero to +100 mmHg and zero to -75 mmHg have been recorded. Observations were made in arterioles, terminal arterioles, and precapillary sphincters in the wing web of intact, unanesthetized bats. The results show for all categories of vessels that with reduced transmural pressures there is a progressive increase in mean diameter and a decrease in rhythmic vasomotion rate. Flow changes are variable. For elevated transmural pressures there is a vasoconstriction with drastic flow reduction that is inconsistent with metabolic control. However, after prolonged elevation of pressure there is a progressive increase in flow, suggesting a "metabolic escape". Computed wall tension remains reasonably constant for a wide range of transmural pressures, suggesting that wall tension may be the controlled variable. These findings support the hypothesis of a myogenic reaction as a mechanism for maintenance of basal vascular tone in the intact unanesthetized bat.