Pressor response

Much of the pulmonary NEP activity is believed to reside in the epithelium, as has been demonstrated in the ferret (Borson et al., 1986), and thus it is likely that inhaled ozone would preferentially destroy luminal NEP before affecting any enzymes in the vasculature, which may degrade peptides delivered by the intravenous route. This may explain the route-dependency of BHR after ozone in guinea pigs. Further evidence that the oxidant effects of inhaled ozone are selective is provided by the findings that pressor responses to angiotensin I (which requires conversion by ACE to angiotensin II) were not altered by ozone exposure (Yeadon et eU., 1992). 

J. Enhanced pressor response to angiotensin I in normotensive men with the deletion genotype (DD) for angiotensinconverting enzyme. Hypertension 1995 25 1266-1269. 

Paradoxical pressor response Paradoxical pressor response has been reported with IV methyidopa. 

Cardiovascular The hyperdynamic circulation caused by hydralazine may accentuate specific cardiovascular inadequacies. It may reduce the pressor responses to epinephrine. Postural hypotension may result from hydralazine. Use with caution in patients with cerebral vascular accidents. 

Possible adverse reactions include headache anorexia nausea vomiting diarrhea palpitations tachycardia angina pectoris toxic reactions (particularly the LE cell syndrome) lacrimation conjunctivitis dizziness tremors psychotic reactions rash urticaria pruritus fever chills arthralgia eosinophilia constipation paralytic ileus lymphadenopathy splenomegaly nasal congestion flushing edema muscle cramps hypotension paradoxical pressor response dyspnea urination difficulty ... 

EtOH i pressor response W/ epi i effects W/ NSAIDs EMS Some formulations contain a preservative that can cause anaphylactic Rxns can cause lupus-like erythematosus (muscle pain, fever, rash) use other antihypertensives/diuretics w/ caution concurrent EtOH use T effects OD May cause profound hypotension, HA and tach give IV fluids activated charcoal may be effective... 

Isosorbide Dinitrate Hydralazine (BiDil) [Antianginal, Antihypertensive/Vasodilator, Nitrate] Uses HF in African Amer-icans improve survival functional status, prolong time between hospitalizations Action Relaxes vascular smooth muscle peripheral vasodilator Dose Initially 1 tab tid PO (if not tol ated reduce to 1/2 tab tid), titrate >3-5 d as tolerated Max 2 tabs tid Caution [C, /-] recent MI, syncope, hypovolemia, hypotension, hep impair Contra For children, concomitant use w/ PDE5 inhibitors (sildenafil) Disp Tabs SE HA, dizziness, orthostatic hypotension, sinusitis, GI distress, tach, paresthesia, amblyopia Interactions t Risk of severe hypotension W/ antihypertensives, ASA, CCBs, MAOIs, phenothiazides, sildenafil, tadalafil, vardenafil, EtOH X pressor response Wf i -1- effects W7 NSAIDs EMS Use ASA, antihypertensives and CCBs w/ caution, may t hypotension concurrent Viagra-type drug use can lead to profound hypotension concurrent EtOH use can t effects OD May cause N/V, profound hypotension, skin flushing, HA from ICP, bradycardia, confusion, and circulatory collapse activated charcoal may be effective, epi use is contraindicated... 

Phenylephrine is not a substrate for COMT, while metaraminol and methoxamine are not metabolized by either COMT or MAO. Consequently, their duration of action is considerably longer than that of norepinephrine. Following intravenous injection, pressor responses to phenylephrine may persist for 20 minutes, while pressor responses to metaraminol and methoxamine may last for more than 60 minutes. 

Absolute selectivity of action for i- or a2-receptors does not exist for any available a-agonists and antagonists. Furthermore, as is the case with (3-receptors, a given effector tissue may contain more than one a-receptor subtype. Recent evidence suggests that in addition to ai-receptors, vascular smooth muscle may possess a2-receptors. Although the functional importance of a2-re-ceptors in blood vessels seems to be less than that of aj-receptors, this can account for certain clinical observations, as for example the pressor response that occurs upon initiation of treatment with the az-agonist clonidine. 

The associated initial release of catecholamines may result in an excessive pressor response and stimulation of cardiac force and pacemaker activity. The resulting increase in myocardial oxygen consumption in a patient with ischemic heart disease may lead to ischemic pain (angina pectoris). Patients in a state of circulatory shock probably should not be administered bretylium because of its delayed sympatholytic action. 

The administration of a bolus dose of adenosine is associated with a biphasic pressor response. There is an initial brief increase in blood pressure followed by vasodilation and secondary tachycardia. 

An acute intravenous injection of clonidine may produce a transient pressor response that apparently is due to stimulation of peripheral vascular a-receptors. The pressor response does not occur after oral administration, because the drug s centrally mediated depressor action overrides it. 

Hypotensive activity. Essential oil, administered intravenously to dogs at a dose of 3 p,L/kg, was active. The ethanol (70%) extract, administered intravenously to dogs at a dose of 75 mg/kg, was active. There was a dip followed by rise in blood pressure° . Ethanol (80%) extract of the aerial parts, at a dose of 10 mg/kg, was not blocked by atropine. The extract did not inhibit pressor response of norepinephrine either . Ethanol (95%) extract of the seed, administered intravenously to dogs at a dose of 10 mg/kg, produced a transient effect that was blocked by atropine ". Petroleum ether fraction chromatographed and fraction eluted with chloroform, administered intravenously to rabbits at a dose of 0.80 mg/kg, was inactive. Methanol extract, administered intravenously to dogs and rabbits at a... 

Cardiovascular effect. [6]-shogaol, administered intravenously to rats at a dose of 0.5 mg/kg, produced a rapid fall in blood pressure, bradycardia, and apnea. There was a marked pressure pressor response in blood pressure that occurred after the rapid fall. A dose of 3.6 pM produced inotropic and chronotropic actions on isolated atria in rats. The effect disappeared by repeated injections or pretreatment of 100 mg/kg administered subcutaneously ° k Intravenous doses of 0.1 to 0.5 pg produced a pressor response in a dose dependent manner. The response was markedly reduced by spinal destruction at the sacral cord level. Norepinephrine (10 pg/kg, intravenously) induced pressor response that was not affected by spinal destruction. In rats in which the spinal cord was destroyed at the thoracic cord level, [6]-shogaol-induced pressor response was reduced by hexamethonium (10 mg/kg, intravenously) and phentolamine (10 mg/ kg, intravenously). When the spinal cord was destroyed at the sacral level, the pressor response was not affected by these blockades. In the hindquarters of rats that were perfused with rat s blood, [6]-shogaol produced two pressor responses on the perfusion pressure. The first was accompanied by a rise in systemic blood pressure, was re-... 

Suekawa, M., M. Aburada, and E. Hosoya. Pharmacological studies on ginger. 111. Effect of the spinal destruction on (6)-shogaol induced pressor response in rats. J Pharmacobiodyn 1986 9(10) 853-860. 

Mechanism of Action A sympathomimetic amine that produces CNS and respiratory stimulation, mydriasis, bronchodilation, a pressor response, and contraction of the urinary sphincter Directly effects alpha and beta receptor sites in peripheral system. Enhancesreleaseof norepinephrine by blocking reuptake, inhibiting monoamine oxidase. Therapeutic Effect Increases motor activity, mental alertness decreases drowsiness, fatigue. 

Mild to moderate hypotension SC,1M 2-5mg(range 1-10 mg), repeated no more than every 10-15 minutes. Maximum initial dose 5 mg. IV 0.2 mg (range 0.1 to 0.5 mg), given no more frequently than every 10-15 minutes. Maximum initial dose 0.5 mg. Severe hypotension, severe shoch IV Initially, 100-180 mcg/minlVinfusion,withdose titration to the desired MAP and SVR. A maintenance infusion rate of 40-60 mcg/min IV is usually adequate after blood pressure stabilizes. If necessary to produce the desired pressor response, additional phenylephrine in increments of 10 mg or more may be added to the infusion solution and the rate of flow adjusted according to the response of the patient. 

Vasoconstriction in regional anesthesia IV The manufacturer states that the optimum concentration of phenylephrine HCl is 0.05 mg/ml (1 20,000). Solutions maybe prepared for regional anesthesia by adding 1 mg of phenylephrine HCl to each 20 ml of local anesthesia solution. Some pressor response can be expected when at least 2 mg is injected. 

It is a vasopressor agent with some structural similarity to adrenaline and has a powerful alpha receptor stimulant action. The pressor response is accompanied by reflex bradycardia. It is used as a nasal decongestant and mydriatic agent and also in the treatment of paroxysmal supraventricular tachycardia. 

Alpha blockers are the drugs which block the pressor response to noradrenaline and... 

It has low affinity for adrenergic, cholinergic, histaminic, dopaminergic, and serotoninergic receptors ( 176). At a dose of 4 mg twice daily, reboxetine has exerted substantial inhibition of NE uptake in humans as witnessed by abolishment of the tyramine pressor response ( 177). 

After intravenous injection, clonidine produces a brief rise in blood pressure followed by more prolonged hypotension. The pressor response is due to direct stimulation of partial agonist at a receptors because it also inhibits pressor effects of other agonists. 

Ang II is a very potent pressor agent—on a molar basis, approximately 40 times more potent than norepinephrine. The pressor response to intravenous Ang II is rapid in onset (10-15 seconds) and sustained during long-term infusions. A large component of the pressor response is due to direct contraction of vascular—especially arteriolar—smooth muscle. In addition, however, Ang II can also increase... 

Potent peptide antagonists of the action of Ang II are available. The best-known of these is the partial agonist, saralasin. Saralasin lowers blood pressure in hypertensive patients but may elicit pressor responses, particularly when circulating Ang II levels are low. Because it must be administered intravenously, saralasin is used only for investigation of renin-dependent hypertension and other hyperreninemic states. 

Endothelins exert widespread actions in the body. In particular, they cause dose-dependent vasoconstriction in most vascular beds. Intravenous administration of ET-1 causes a rapid and transient decrease in arterial blood pressure followed by a prolonged increase. The depressor response results from release of prostacyclin and nitric oxide from the vascular endothelium, whereas the pressor response is due to direct contraction of vascular smooth muscle. Endothelins also exert direct positive inotropic and chronotropic actions on the heart and are potent coronary vasoconstrictors. They act on the kidneys to cause vasoconstriction and decrease glomerular filtration rate and sodium and water excretion. In the respiratory system, they cause potent contraction of tracheal and bronchial smooth muscle. 

Sympathomimetics [P] Increased pressor response to norepinephrine, epinephrine, and phenylephrine. 

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