Arteriolar constriction

Abnormalities in either the renal or tissue autoregulatory processes for sodium excretion, plasma volume, and arteriolar constriction ... 

With advancing age, the patient with essential hypertension progressively changes his hemodynamic pattern into one of normal cardiac output with increased peripheral arteriolar constriction and, finally, later in the natural course of the disease into one of lower cardiac output and further increase in peripheral vascular resistance ). 

Injection Slow infusion of injection is preferable to bolus administration. Rapid infusion of digitalis glycosides has been shown to cause systemic and coronary arteriolar constriction, which may be clinically undesirable. Caution is thus advised and injection probably should be administered over a period of 5 minutes or more. Mixing injection with other drugs in the same container or simultaneous administration in the same intravenous line is not recommended. 

If the pH remains above 7.55, as in severe alkalosis, arteriolar constriction may lead to reduced cerebral blood flow, tetany, seizure or, potentially, death. 

A first report conducted in an in vivo seizure model in mice indicates that stimulation of A3AR protects from seizures (von Lubitz et al. 1995). Acute systemic administration of IB-MECA protects against chemically-induced (NMDA injection) but not electrically-induced seizures while a protective effect of chronically administered IB-MECA is evident in both chemically- and electrically-evoked seizures (von Lubitz et al. 1995). The protective effect of acute administration of IB-MECA is attributed to both arteriolar constriction and severe hypotension (von Lubitz et al. 1994), which can reduce the final intracerebral concentration of the chemoconvulsant NMDA (von Lubitz et al. 1995). In a study conducted on seizure-sensitive DBA/2 mice, an animal model of generalized... 

Further in vivo studies revealed that the arteriolar constriction that follows mast cell activation via inosine, is the result of histamine and thromboxane release and that A3AR is involved in mediating this response (Shepherd and Duling 1996 Shepherd et al. 1996 Fozard et al. 1996 Reeves et al. 1997). Inosine, which does not bind to Aj or A2 receptors, thus elicits a monophasic arteriolar constrictor response distinct from the multiphasic dilator/constrictor response to adenosine (Jin et al. 1997). 

Merely because a substance depresses blood pressure does not make it a true antihypertensive substance. The level of blood pressure is the resultant of several factors the viscosity of the blood, the cardiac output, the volume of circulating blood, and the state of the arterial and arteriolar bed, which determines the peripheral resistance to blood flow, other factors being equal. This discussion has indicated that peripheral resistance through arteriolar constriction may be affected by renal blood flow and the production of circulating pressor agents. Therefore, a definition of a true antihypertensive substance is necessary, in order that we be not misled by depressor substances which lower blood pressure at a detriment to the body s economy. 

Figure 1 shows the effect of traumatic or unpleasant interview on blood pressure, cardiac stroke volume, renal blood flow, and the fraction of the renal blood flow that was filtered at the glomeruli (filtration fraction). In response to the interview both the systolic and diastolic blood pressure and the stroke volume of the heart increased. There was a decrease in the flow of blood through the kidney, and this decrease was due predominantly to an efferent arteriolar constriction since the filtration fraction was increased somewhat. 

In the rabbit, delta opioid receptors may have a role in protecting the enterohepatic system from ischemic injury [151]. This effect may be related to the presynaptic inhibition of mesenteric arteriolar constriction and consequent preservation of blood flow by delta opioid agonists [152], However, vasoactive effects of opioids mediated by delta opioid receptors are not observed in the rat [153,154]. Delta-opioid receptors have a similar protective action in the myocardium, which is described in detail elsewhere in this volume. 

SAFETY PROFILE Human poison by unspecified routes. Moderately toxic to humans and experimentally by ingestion. Experimental poison by intravenous, intraperitoneal, and subcutaneous routes. An experimental teratogen. Human systemic effects by ingestion coma, blood pressure decrease, regional or general arteriolar constriction, dyspnea, cyanosis, respiratory depression, nausea or vomiting, and allergic skin dermatitis. Experimental reproductive effects. Mutation data reported. Implicated in aplastic anemia. Used as a tranquilizer. When heated to decomposition it emits toxic fumes of NOx. See also CARBAMATES. 

Midodrine is a prodrug, whose active metabolite is relatively selective for vascular postjunctional alphai-adrenoceptors and therefore increases peripheral resistance by arteriolar constriction, with some veno-constriction in capacitance vessels (1). It has minimal activity in the central nervous system, since it does not cross the blood-brain barrier. It can be given orally and has a systemic availabihty of over 90% by this route. The half-life of the active deglycinated metabolite is relatively short (2-3 hours). The dosage range is 2.5-10 mg tds, and is usually toward the upper end of this range. 

Renal nerve stimulation Afferent-tefferent arteriolar constriction [245]... 

Cyclosporine interlobular, afferent and efferent arteriolar constriction Vasoconstriction due to altered NO metabolism [250] [251]... 

Staurosporine Does not alter the effect of mibefradil (T-type calcium channel blocker) to dilate angiotensin ll-induced arteriolar constriction. [261]... 

Munger KA,Takahashi K, Awazu M, Frazer M, Falk SA, Conger JD, Badr KF Maintenance of endothelin-induced renal arteriolar constriction in rats is cyclooxygenase dependent. Am.J.Physiol 264 F637-F644,1993... 

TakenakaT, KannoY, KitamuraY, Flayashi K, Suzuki FI, SarutaT Role ofchloride channels in afferent arteriolar constriction. Kidney Int 50 864-872,1996... 

Patients at greatest risk are those dependent on angiotensin 11 to maintain Wood pressure and renal efferent arteriolar constriction. These include patients with hemodynamicaUy significant renal artery stenosis, particularly bilateral stenosis, and those with decreased effective arterial renal blood flow, particularly those with congestive heart failure, volume depletion from excess diuresis or gastrointestinal fluid loss, hepatic cirrhosis with ascites, and the nephrotic syndrome." ... 

The peptidoleukotrienes play a major role in the pathophysiological sequelae of anaphylaxis by exerting profound effects on smooth muscle tone. Peptidoleukotrienes contract respiratory, vascular, and intestinal smooth muscle. Furthermore, peptidoleukotrienes have potent effects on the cardiovascular system including coronary vasoconstriction, reduced heart rate, arteriolar constriction, venule dila-... 

Tomoda et al.157 reported on altered renal response to enhanced endogenous serotonin after tryptophan administration in essential hypertension in human subjects. The altered renal response (renal plasma flow, glomerular filtration rate) to tryptophan found in essential hypertension was considered to be partly related to the exaggerated efferent arteriolar constriction induced by endogenously formed serotonin. In essential hypertension, there was a baseline overproduction of renal serotonin, which may have contributed to a reduction in renal excretory capability. 

Renal nerve stimulation Afferent -i- efferent arteriolar constriction [311]... 

Contraction of veins forces reserved blood into circulation, which increases diastolic pressure, while the increased circulating blood volume, coupled with arteriolar constriction (which increases the total peripheral resistance), increases systolic pressure. The drug simultaneously causes norepinephrine to be released from sympathetic nerve terminals, which increases cardiac output and antagonizes the effects of vagal compensation. 

Acute changes in cardiac contractility, peripheral resistance, or blood volume may transiently exert differential effects on cardiac output and venous return. Except for such brief disparities, however, such factors simply alter flow around the entire circuit. It is irrelevant whether one thinks of that flow as cardiac output or venous return. All too frequently authors have ascribed the reduction in cardiac output during hemorrhage, for example, to a decrease in venous return. Such an explanation, of course, is a blatant example of circular reasoning, in its most literal sense. Hemorrhage reduces blood flow around the entire circuit, mainly because the diminished blood volume and generalized arteriolar constriction lead to a reduction in the cardiac preload. To attribute the reduction in cardiac output to a curtailment of venous return is equivalent to ascribing the decrease in systemic blood flow to a decrease in systemic blood flow ... 

Messina EJ, Sun D, Roller A, Wolin MS, Kaley G. Increases in oxygen tension evoke arteriolar constriction by inhibiting endothelial prostaglandin synthesis. Microvasc Res 1994 48 151-160. 

Arterioles The primary effect of 1/R on arterioles is impaired endotheUum-dependent relaxation of vascular smooth muscle. The net result is arteriolar constriction and reduced blood flow, which may promote organ injury. ROS generation during reperfusion appears to be the underlying cause of this response, as antioxidants attenuate 1/R-induced arteriolar constriction. The specific oxidant involved is superoxide, which interacts with NO, such that levels of this endothelial-derived dilator are reduced during reperfusion. 

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