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Hypotensive action

Mention must be made of the u.se of o- or p-hydroxystyryl thiazolo dyes as indicators for protolytic titrations in nonaqueous media (145). and of the hypotensive action of some neotrinuclear thiazolo cyanines in experiments on animals (146). [Pg.80]

Of the alkaloids of the han-fang-chi group of drugs (p. 350), Ohta states that kukoline is a strong reflex and spasm stimulant and finally causes paralysis and death. Raymond-Hamet states that it suppresses the hypotensive action of dihydroxyphenylethanolethylamine. [Pg.362]

A preliminary report on rauwolscine by Chakravarti indicates that it is a cardiovascular depressant, shows hypotensive action and a relatively high toxicity. Koepfli s rauwolfine produces a fall in blood pressure, and stimulation of respiration in frogs it has a curare-like action. The rauwolfine of van Itallie and Steenhauer has been examined by Hartog and by de Boer, especially in regard to its cardiac action. According to Raymond-Hamet, it reverses the action of adrenaline. [Pg.765]

VMATs are irreversibly inhibited by the potent antihypertensive drug reserpine. The depressive effects of reserpine helped to formulate the original monoamine hypothesis of affective disorders. Reseipine also appears to interact with the transporters near the site of substrate recognition. Tetrabenazine, which is used in treatment of movement disorders, inhibits VMAT2 much more potently than VMAT1, consistent with the less hypotensive action of this agent. [Pg.1282]

Varga KLK, Martin BR, Kunos G. Novel antagonist implicates the CB1 receptor in the hypotensive action of anandamide. Eur J Pharmacol 1995 278 279-283. [Pg.135]

The answer is b. (Hardman, p 790.) Neuronal uptake is necessary for the hypotensive action of guanethidine. It competes for the norepinephrine storage site and, in time, replaces the natural neurotransmitter. This is the basis of its hypotensive effect. Drugs that prevent reuptake by the neurons, such as cocaine, would destroy the effectiveness of guanethidine... [Pg.124]

Nitroprusside is the agent of choice for minute- to-minute control in most cases. It is usually given as a continuous IV infusion at a rate of 0.25 to 10 mcg/kg/min. Its onset of hypotensive action is immediate and disappears within 1 to 2 minutes of discontinuation. When the infusion must be continued longer than 72 hours, serum thiocyanate levels should be measured, and the infusion should be discontinued if the level exceeds 12 mg/dL. The risk of thiocyanate toxicity is increased in patients with impaired kidney function. Other adverse effects include nausea, vomiting, muscle twitching, and sweating. [Pg.141]

Compared with Molsidomine, both SIN-1 and SIN-1A are reported to induce similar, but more rapid hypotensive action [95, 96]. SIN-1A, after undergoing oxidation in the presence of oxygen or, in vivo, possibly by redox-active enzymes such as cytochrome C [97, 98] or by reaction with ferric myoglobin formed during reperfusion injury [99], releases NO through an intermediate radical cation. [Pg.159]

The hypothesis that HNO is not involved during NO-release from sydnonimines was confirmed by the study of NO-release from C78-0652 109, the dimethyl derivative of SIN-1A (Scheme 6.19). This product closely resembles SIN-1A in its biological and pharmacological behavior, showing a clear NO-dependent vasodilating effect on guinea pig pulmonary arteries and hypotensive action in anesthetized and conscious dog models [105]. [Pg.159]

There is interest in the possible use of other metal nitrosyl complexes as vasodilators, but from the series KJM(CN)6NO] where M = V, Cr, Mn, and Co (n = 3) or M = Mo (n = 4) neither the Cr nor the Mn complexes exhibit any hypotensive action (504). Iron-sulfur-nitrosyl clusters such as [Fe4S4(NO)4] are active, and their effects can be potentiated by visible light (505). [Pg.266]

Mode-of-Action Hypotheses. May we now turn to consider some of the suggested mechanisms put forward to explain the hypotensive action of the 3-blocking drugs and see if any are compatible with the clinical and pharmacological data. Before doing so however, it perhaps would be useful to summarise the characteristics of the anti-hypertensive action of the drugs. [Pg.17]

The relevance of either the experimentally demonstrated central hypotensive action of the 3-blockers, or their ability to antagonise sympathetically mediated renin release remains to be proven. While it is still possible that the mechanism of the anti-hypertensive action of the 3-blocking drugs could contain both a central and a renin-inhibitary component, the clinical evidence would appear to rule against the possibility of either being a major component of the mode-of-action. [Pg.25]

The hypotensive action of clonidine could not be explained satisfactorily by effects on the peripheral circulation. Numerous studies therefore considered the possibility of an effect on the central nervous system. Investigations performed on spinalized animals could... [Pg.31]

The relation between the dosage, plasma concentration, and hypotensive action of hydrallazine has recently been examined (Zl). This drug, despite its many advantages as a hypotensive agent, fell from favor because of an unacceptably high incidence of severe side effects. Studies by Perry et al. (P8) have shown, however, that slow acetylators are more liable to develop the severe lupuslike syndrome associated with hydrallazine usage than fast acetylators. [Pg.92]

Zl. Zacest, R., and Koch-Weser, J., Relation of hydralazine plasma concentration to dosage and hypotensive action. Clin. Pharmacol. Ther. 13, 420-425 (1972). [Pg.109]

Clonidine is a selective o -adrenergic agonist. Clonidine has expressed hypotensive action, which is associated with a reduction of general peripheral vascular resistance, reduced frequency of cardiac beats, and a reduction of cardiac output. The mechanism of action of clonidine is caused by stimulation of o -adrenoreceptors of the inhibitory structures of the brain as well as a reduction of sympathetic impulses to the blood vessels and brain. [Pg.153]

Clonidine is a selective Oj-adrenergic agonist that exhibits pronounced hypotensive action that is associated with a reduction of overall peripheral vascular resistance, decline in frequency of cardiac contraction, and reduced cardiac output. Clonidine is the drug of choice for treating various degrees of hypertension when used in combination with oral diuretics. [Pg.299]

Methyldopa is an a-methoxylated derivative of levodopa that exhibits hypotensive action by reducing overall peripheral vascular resistance and reducing heart work. Antihypertensive action of methyldopa consists of the biotransformation of methyldopa into methylnoradrenaline (methylnorepinephrine), which acts as a pseudo neurotransmitter. The current, universally accepted point of view is that the action of methyldopa is carried out through the CNS, where methylnorepinephrine, a powerful stimulant of a-adrenergic receptors of the medulla, inhibits the vasomotor center. [Pg.300]

Because of the anticholinergic action of these agents, use with caution and with appropriate monitoring in patients with glaucoma, obstructive disease of the Gl or GU tract, and in elderly males with possible prostatic hypertrophy. These drugs may have a hypotensive action, which may be confusing or dangerous in postoperative patients. [Pg.983]

Diazoxide lowers blood pressure within 3 to 5 minutes after rapid intravenous injection, and its duration of action may be 4 to 12 hours. Interestingly, if diazoxide is either injected slowly or infused its hypotensive action is quite modest. This is believed to be due to a rapid and extensive binding of the drug to plasma proteins. Both the liver and kidney contribute to its metabolism and excretion. The plasma half-life is therefore prolonged in patients with chronic renal failure. [Pg.230]

The onset of the hypotensive action of sodium nitroprusside is rapid, within 30 seconds after intravenous administration. If a single dose is given, the action lasts for only a couple of minutes. Therefore, sodium nitroprusside must be administered by continuous intravenous infusion. After the infusion is stopped, blood pressure returns to predrug levels within 2 to 3 minutes. [Pg.230]


See other pages where Hypotensive action is mentioned: [Pg.153]    [Pg.202]    [Pg.530]    [Pg.332]    [Pg.333]    [Pg.133]    [Pg.217]    [Pg.220]    [Pg.264]    [Pg.31]    [Pg.125]    [Pg.140]    [Pg.141]    [Pg.170]    [Pg.174]    [Pg.92]    [Pg.309]    [Pg.177]    [Pg.153]    [Pg.324]    [Pg.336]    [Pg.581]    [Pg.115]   
See also in sourсe #XX -- [ Pg.200 , Pg.207 , Pg.209 ]

See also in sourсe #XX -- [ Pg.28 , Pg.30 , Pg.200 , Pg.207 , Pg.209 , Pg.787 ]

See also in sourсe #XX -- [ Pg.787 ]

See also in sourсe #XX -- [ Pg.76 , Pg.79 , Pg.93 ]




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