Vasodilation causing

The answer is d. (Hardman, p T36J The addition of a vasoconstrictor, such as epinephrine or phenylephrine, to certain short-acting, local anesthetics is a common practice in order to prevent the rapid systemic absorption of the local anesthetics, to prolong the local action, and to decrease the potential systemic reactions. Some local anesthetics cause vasodilation, which allows more compound to escape the tissue and enter the blood. Procaine is an ester-type local anesthetic with a short duration of action due to rather rapid biotransformation in the plasma by cholinesterases. The duration of action of the drug during infiltration anesthesia is greatly increased by the addition of epinephrine, which reduces the vasodilation caused by procaine. 

C. The vasodilation caused by bradykinin, histamine, hydralazine, and acetylcholine depends in part upon nitric oxide release from the endothelium. Minoxidil activates K+ channels, which results in vascular smooth muscle hyperpolarization and thereby relaxation. 

Although diuretics are often successful as monotherapy, they also play an important role in patients who require multiple drugs to control blood pressure. Diuretics enhance the efficacy of many agents, particularly ACE inhibitors. Patients being treated with powerful vasodilators such as hydralazine or minoxidil usually require simultaneous diuretics because the vasodilators cause significant salt and water retention. 

The peripheral nervous system effects are considered as under-stimulation of the end organs. This decreased stimulation of eccrine and apocrine sweat glands in the skin results in dry skin and a dry mouth, and is considered dry as a bone . The reduction in the ability to dispel heat by evaporative cooling decreases sweating, and the compensatory cutaneous vasodilation causes the skin to become warm or hot as a hare and red as a beet . This is similar to the atropine flush. The decreased heat loss also results in an increased core temperature. 

Benziodarone, a coronary vasodilator, causes in vitro inhibition of the BSP conjugating system. This drug increases the retention of BSP in plasma but has no effect on the retention of phenol dibromophthalein disulfonate, which is not conjugated. Benziodarone probably acts specifically on the conjugating enzyme since it has been shown to inhibit other conjugations with glutathione (B38). 

Amyl nitrite is a highly volatile liquid that is sold in fragile glass ampules packaged in a protective cloth covering. The ampule can be crushed, which causes the rapid release of inhalable vapors. Amyl nitrite has a rapid onset of action, and its duration of action is 8 to 10 minutes. The pronounced vasodilation causes tachycardia, enhanced cardiac output, and vasoconstriction. Amyl nitrite is no longer used for the control of angina. 

Propranolol and other nonselective receptor antagonists inhibit the vasodilation caused by isoproterenol and augment the pressor response to Epi. This action is significant in patients with pheochromocytoma, in whom [ receptor antagonists should be used only after adequate a receptor blockade has been established. This sequence avoids uncompensated a receptor-mediated vasoconstriction caused by catecholamines secreted by the tumor. 

When used as a heart medication, nitroglycerin is administered in the form of a pill, patch, or intravenous solution. Nitroglycerin works in the body by releasing nitric oxide, a vasodilator. Vasodilators cause the smooth muscle surrounding blood vessels to relax, allowing the vessels to expand and improve the flow of blood. The drug is often taken when the pain of angina or a heart attack is first noticed. 

DKA usually develops over a short period of time, generally in less than 24 h. There may have been some antecedent days with general malaise and poor metabolic control. Depending on the degree of hyperglycaemia, the history will include symptoms of polydipsia and polyuria. Specific symptoms depend on precipitating factors and co-morbidity. Physical examination may reveal poor skin turgor, hyperventilation (Kussmaul), hypotension, tachycardia and impairment of mental status. Many patients have infection, but patients may present with normothermia or even hypothermia due to peripheral vasodilation caused by the acidemia. 

Beckman JA, Goldfine AB, Gordon MB, Garrett LA, Creager MA. Inhibition of protein kinase Cbeta prevents impaired endothelium-dependent vasodilation caused by hyperglycemia in humans. Circ Res 2002 90 107-111. 

Trlvastal, E-k95, (V) is primarily a vasodilator causing selective increase in femoral blood flow while decreasing splanchnic flow. It caused a reduction in blood pressure, heart rate and respiration which was liihlbited by vagotomy. ... 

The vasoactive kinins and the peptides of the complement system are examples of the short-chain peptide mediators [165]. Bradykinin is formed by the action of the enzyme kallikrein on the plasma protein, a2-macroglobulin [171]. The resulting nonapeptide is a potent vasodilator, causing erythema, swelling, and pain [172]. Additionally, bradykinin activates phospholipase A2, the enzyme responsible for generating the precursor to the lipid mediators [173]. 

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