Coronary vasoconstriction

Hattori Y, Levi R Effect of PGDj on cardiac con- 43 tractihty a negative inotropism secondary to coronary vasoconstriction conceals a primary positive inotropic action. J Pharmacol Exp Ther 1986 237 ... 

Phenylephrine 10-1000 pg/minute Seconds Bradycardia, coronary vasoconstriction, decreased renal perfusion, metabolic acidosis Alpha-1, increased cardiac output (CO), decreased systemic vascular resistance (SVR)... 

Decreased HR, contractility, and blood pressure reduce MVo2 and oxygen demand in patients with effort-induced angina. j3-Blockers do not improve oxygen supply and, in certain instances, unopposed a-adrenergic stimulation may lead to coronary vasoconstriction. 

ADH, a nonapeptide, released from the posterior pituitary gland promotes re-absorption of water in the kidney. This response is mediated by vasopressin receptors of the V2 subtype. ADH enhances the permeability of collecting duct epithelium for water (but not for electrolytes). As a result, water is drawn from urine into the hyperosmolar inter-stitium of the medulla. Nicotine augments (p. 110) and ethanol decreases ADH release. At concentrations above those required for antidiuresis, ADH stimulates smooth musculature, including that of blood vessels ( vasopressin ). The latter response is mediated by receptors of the Vi subtype. Blood pressure rises coronary vasoconstriction can precipitate angina pectoris. Lypres-sin (8-L-lysine vasopressin) acts like ADH. Other derivatives may display only one of the two actions. 

Large doses - Large doses raise arterial pressure, produce coronary vasoconstriction, and slow the heart by both a direct action and a vagal effect. 

Urine alkalinization is a treatment modality that increases elimination of poisons by the intravenous administration of sodium bicarbonate to produce urine with a pH of more than or equal to 7.5 and must be supported by high urine flow. This technique might be useful for the elimination of drugs with an acid pKa such as salicylates (but not recommended for phenobarbital intoxication for which multiple-dose activated charcoal is better), chlorpropamide, 2,4-dichlorophenoyacetic acid, diflunisal, fluoride, mecoprop, methotrexate. Complications include severe alkalemia, hypokalemia, hypocalcemia and coronary vasoconstriction. 

Rubanyi G, Ligeti L, Roller A, et al. 1984. Possible role of nickel ions in the pathogenesis of ischemic coronary vasoconstriction in the dog heart. J Mol Cell Cardiol 16 533-546. 

Sumatriptan Partial agonist at 5-HT1B/1D receptors Effects not fully understood may reduce release of calcitoningene-related peptide and perivascular edema in cerebral circulation Migraine and cluster headache Oral, nasal, parenteral duration 2 h Toxicity Paresthesias, dizziness, coronary vasoconstriction Interactions Additive with other vasoconstrictors... 

Particle-induced coronary vasoconstriction in the rat heart Pharmacological investigation of underlying mechanisms, Thorac. Cardiovasc. Surg., 34, 316-325. 

Coronary vasoconstriction has been demonstrated for major epicardial coronary arteries (7) and for the small intramural coronary resistance vessels (8) and may occur because of local vasoconstrictors derived from platelets present in the thrombus, such as serotonin, thromboxane A2, and thrombin. 

Togni M, Windecker S, Cocchia R, et al, Sirolimus-eluting stents associated with paradoxic coronary vasoconstriction. J Am Coll Cardiol 2005 46 23 1-236. 

Dual inhibitors also demonstrate other therapeutical benefits. They reduced the coronary vasoconstriction in arthritic hearts in a rat model [101], and significantly decreased angiotensin II-induced contractions in human internal mammary artery [102], Opioid receptor activation can cause a presynaptic inhibition of neurotransmitter release mediated by LOX metabolites of arachidonic acid in midbrain neurons. The efficacy of opioids was enhanced synergistically by treatment of brain neurons with COX and LOX dual inhibitors. This report might lead to development of CNS analgesic medications involving combinations of lowered doses of opioids and COX/LOX dual inhibitors [103]. The COX and 5-LOX dual inhibitors also can prevent lens protein-induced ocular inflammation in both the early and late phases [104]. 

Myocardial ischemia was reported in a fit 29-year-old patient after the nasal application of cocaine for surgery. No relief was gained from vasodilators or intracoronary verapamil, and there were no other signs of cocaine toxicity. Although coronary vasoconstriction and platelet activation are systemic effects of cocaine, pre-existing thrombus may also have played a part (SEDA-22,142). 

Lange RA, Cigarroa RG, Flores ED, McBride W, Kim AS, Wells PJ, Bedotto JB, Danziger RS, Hillis LD. Potentiation of cocaine-induced coronary vasoconstriction by beta-adrenergic blockade. Ann Intern Med 1990 112(12) 897-903. 

Boehrer JD, Moliterno DJ, Willard JE, Hillis LD, Lange RA. Influence of labetalol on cocaine-induced coronary vasoconstriction in humans. Am J Med 1993 94(6) 608-10. 

Reduction of portal pressure. Vasopressin (anti-duiretic hormone, see p. 711), in addition to its action on the renal collecting ducts (through receptors), constricts smooth muscle (Vj receptors) in the cardiovascular system (hence its name), and particularly in splanchnic blood vessels, so reducing blood flow in the portal venous system. Unfortunately, coronary vasoconstriction can also occur, and treatment has to be withdrawn from 20% of patients because of myocardial ischaemia. Glyceryl trinitrate (transdermally, sublingually, or intravenously) reduces the cardiac risk and, advantageously, further reduces portal venous resistance and pressure. 

Nolte CW, lost S, Mugge A, Daniel WG. Protection from digoxin-induced coronary vasoconstriction in patients with coronary artery disease by calcium antagonists. Am J Cardiol 1999 83(3) 440-2. 

Seven triptans have been compared and rated as generally very well tolerated (10). Naratriptan, almotriptan, and frovatriptan were considered to have the best safety profiles, although the differences are minor. Coronary vasoconstriction is a potential risk of the entire class, but the risk is minimal in the absence of coronary artery disease or uncontrolled hypertension significant vascular disease is therefore a hazard of using any of the triptans. Patient preference, however, appears to be more closely related to efficacy than to tolerance. 

Coronary vasoconstriction is a potential risk of all triptans, but the risk is minimal in the absence of coronary artery disease or uncontrolled hypertension. Chest tightness and pain are reported in up to 15% of patients taking sumatriptan and are presumed to be due to vasoconstriction of the coronary arteries. Myocardial infarction has been reported and as a consequence sumatriptan should not be used in patients with cardiovascular disease (11). Intravenous sumatriptan causes some coronary vasoconstriction during diagnostic angiography. Myocardial infarction occurred in a patient who had received sumatriptan 6 mg subcutaneously, but the causal association was not clear. 

Altered coronary blood flow Coronary vasoconstriction or obstruction... 

The KO models confirm the essential adaptive roles of oq-ARs in the heart, where the A and the B are required for chronic trophic or nutritional effects that depend ultimately on anabolic, transcriptional, metabolic, and antiapoptotic processes. The A and the B mediate inotropic effects, which depend on the preparation, and the D causes coronary vasoconstriction. The distinct roles of the A and the B in heart remain to be worked out. Clinically, the results emphasize concern about the use of nonselective oq-antagonist drugs in patients with hypertension or prostate disease. On the other hand, D-selective antagonists might have advantages. 

D Located in brain and arteries (aorta, coronary, mesenteric) Maintain resting BP Vasopressor and hypertensive responses Coronary vasoconstriction... 

G. Heusch, Emerging importance of alpha-adrenergic coronary vasoconstriction in acute coronary syndromes and its genetic background, J Am Coll Cardiol 41, 195-196 (2003). 

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