Vascular smooth muscle, effect

Somlyo AV, Somlyo AP 1971 Strontium accumulation by sarcoplasmic reticulum and mitochondria in vascular smooth muscle. Science 174 955-958 Somlyo AV, Bond M, Somlyo AP, Scarpa A 1985 Inositol-trisphosphate induced calcium release and contraction in vascular smooth muscle. Proc Natl Acad Sci 82 5231-5235 Somlyo AV, Horiuti K, Trentham DR, Kitazawa T, Somlyo AP 1992 Kinetics of Ca2+ release and contraction induced by photolysis of caged D-myo-inositol 1,4,5-trisphosphate in smooth muscle the effects of heparin, procaine, and adenine nucleotides. J Biol Chem 267 22316-22322... 

The Lewis triple response illustrates the effects of histamine on vascular smooth muscle, vascular endothelium, and sensory nerve endings. Intradermal injection of as little as 10 jig histamine produces three distinct effects ... 

Mechanism of Action A prostaglandin that directly affects vascular and ductus arteriosus smooth muscle and relaxes trabecular smooth muscle. Therapeutic Effect Causes vasodilation dilates cavernosal arteries, allowing blood flow to and entrapment in the lacunar spaces of the penis. 

Mechanism of Action An antiasthmatic that binds to cysteinyl leukotriene receptors, inhibiting the effects of leukof rienes on bronchial smooth muscle. Therapeutic Effect Decreases bronchoconstriction, vascular permeability, mucosal edema, and mucus production. 

Mechanism of Action An antianginal and antihypertensive agent that inhibits calcium ion movement across cell membranes, depressing contraction of cardiac and vascular smooth muscle. Therapeutic Effect Increases heart rate and cardiac output. Decreases systemic vascular resistance and BP. 

Additional studies conducted in this laboratory revealed that NO was responsible for the vascular smooth muscle relaxant effects of several different nitro-vasodilators, and that S-nitrosothiols were intermediates in the intracellular formation of NO (Ignarro et al., 1981). We showed also that NO was a potent inhibitor of human platelet aggregation, and that NO elicited such effects by... 

By using drugs that mimic or block the actions of chemical transmitters, we can selectively modify many autonomic functions. These functions involve a variety of effector tissues, including cardiac muscle, smooth muscle, vascular endothelium, exocrine glands, and presynaptic nerve terminals. Autonomic drugs are useful in many clinical conditions. However, a very large number of drugs used for other purposes have unwanted effects on autonomic function. 

The drug at therapeutic dose levels, causes vasodepression which is primarily the outcome of arteriolar dilatation, in order that the ensuing orthostatic hypotension is normally minimal. However, certain extent of venous dilatation invariably occurs, which occasionaly is responsible to afford orthostatic hypotension. It has been duly observed that the smooth muscle-relaxing effects are usually caused due to the hyper-polarization of vascular smooth muscle by activating ATPase-sensitive K-channels. Hence, it is mostly used in IV as a hypotensive drug in situations arising from acute hypertensive crises. 

In addition to the potent natriuretic activity, ANF has significant relaxant effects on vascular and perhaps other smooth muscle tissues.84,110,113,114 Currie observed relaxation of rabbit aorta and chick rectum, which had previously been contracted with epinephrine and carbachol, respectively.8A They use this spasmolytic action to monitor ANF activity and are the first group to separate smooth muscle relaxant activity of similar peptides isolated from cardiac atria, although both peptides are natriuretic.166 A recent report by Winquist et has detailed the vascular smooth muscle relaxing effect of synthetic ANF using a variety of agonists and different vascular smooth muscle preparations.11 Based on these observations, ANF appears to have spasmolytic properties similar to sodium nitroprusside. 

I. Pharmacology. Cimetidine, ranitidine, famotidine, and nizatidine are selective competitive inhibitors of histamine on Hj receptors. These receptors modulate smooth muscle, vascular tone, and gastric secretions and may be involved in clinical effects associated with anaphylactic and anaphylactoid reactions, as well as ingestion of histamine or histamine-like substances (eg, scombroid fish poisoning). Cimetidine, as an inhibitor of cytochrome P-450 enzymes, has been proposed or studied in animals as an agent to block the production of toxic intermediate metabolites (eg, acetaminophen, carbon tetrachloride, halothane. 

Nontraditional Hormones. Novel hormones identified ia cardiovascular tissue have profound effects on maintenance of blood pressure and blood volume ia mammals. Atrial natriuretic hormone (ANH) is a polypeptide hormone secreted from the atria of the heart. When the cardiac atrium is stretched by increased blood volume, secretion of ANH is stimulated ANH ia turn increases salt and water excretion and reduces blood pressure (6). Endothelin is a polypeptide hormone secreted by endothehal cells throughout the vasculature. Although endothelin is released into the circulation, it acts locally in a paracrine fashion to constrict adjacent vascular smooth muscle and increase blood pressure (7). 

Lead is toxic to the kidney, cardiovascular system, developiag red blood cells, and the nervous system. The toxicity of lead to the kidney is manifested by chronic nephropathy and appears to result from long-term, relatively high dose exposure to lead. It appears that the toxicity of lead to the kidney results from effects on the cells lining the proximal tubules. Lead inhibits the metaboHc activation of vitamin D in these cells, and induces the formation of dense lead—protein complexes, causing a progressive destmction of the proximal tubules (13). Lead has been impHcated in causing hypertension as a result of a direct action on vascular smooth muscle as well as the toxic effects on the kidneys (12,13). 

ANPs play an important role in the maintenance of cardiovascular homeostasis by counterbalancing the renin—angiotensin (RAS) system. ANP, the main circulating form of the natriuretic peptides, effectively relaxes vascular smooth muscle, promotes the excretion of sodium and water, and in the CNS inhibits vasopressin release and antagonizes AT-II induced thirst. 

Amiodarone dilates arteriolar vascular smooth muscle, especiady coronary arteries, and thus exhibits antianginal effects. Its effects on the peripheral vasculature to decrease resistance leads to a decrease in left ventricular stroke work and a decrease in myocardial oxygen consumption. The dmg rarely produces hypotension that requires discontinuation of the dmg (1,2). 

Nitroprusside. Nitropmsside is a poteat, fast-actiag vasodilator that has to be administered iatravenously by iafusion. It relaxes arterial and venous vascular smooth muscle. Its use is mainly ia hyperteasive crises. Its effects terminate as sooa as iafusioa of the dmg is stopped. 

In the vasculature, ANG H not only increases contraction of smooth muscle cells, but is also able to induce vascular injury. This can be prevented by blocking NFkB activation [3] suggesting a link between ANG II and inflammation processes involved in the pathogenesis of arteriosclerosis (see below). Thus, ACE inhibitors not only decrease vascular tone but probably also exert vasoprotective effects. 

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