Reserpine hypotension caused

Reserpine, Chlorpromazine and other Psycholeptic Drugs Reserpine depletes postganglionic sympathetic fibres of their noradrenaline and the peripheral sympathetic responses of animals which have been pretreated with reserpine are those which would be expected to follow loss of sympathetic transmitter . Thus, in adrenalectomized, reserpinized cats, stimulation of the splanchnic nerves does not produce the increase in blood pressure which is seen in non-reserpinized animals. Hexamethonium normally produces hypotension due to ganglionic blockade in the reserpinized animal it is without effect. Reserpine also causes a loss of adrenaline from the adrenal medulla. Since this adrenaline is liberated into the blood stream, it is not surprising that reserpine causes hyperglycaemia. 

Theoretically, reserpine might cause hypertension in patients treated with non-selective MAOIs (see Mechanism). On the basis of this the US manufacturer of tranylcypromine contraindicates concurrent use. Conversely, the UK manufacturer of isocarboxazid mentions that it may potentiate the hypotensive effect of reserpine (MAOIs alone can have hypotensive effects). 

Guanethidine, rarely used as a hypotensive drug, also causes some catecholamine depletion, but unlike reserpine it does not cross the blood-brain barrier and thus has no central sedative effects. It acts selectively because it is taken up into the neuron by the same amine pump that transports the neurotransmitter. 

Depletion of peripheral amines probably accounts for much of the beneficial antihypertensive effect of reserpine, but a central component cannot be ruled out. The effects of low but clinically effective doses resemble those of centrally acting agents (eg, methyldopa) in that sympathetic reflexes remain largely intact, blood pressure is reduced in supine as well as in standing patients, and postural hypotension is mild. Reserpine readily enters the brain, and depletion of cerebral amine stores causes sedation, mental depression, and parkinsonism symptoms. 

The stem bark of P. yohimbe (= P. johimbe Corynanthe yohimbe), "yohimbe as it is known in Cameroon, Gabon and Congo is used traditionally as an aphrodisiac and stimulant to prevent sleep (41). The bark contains 1-6% of indole alkaloids, most of which are yohimbane-type alkaloids, the main one being yohimbine [7], which is structurally related to reserpine [8] (89). Yohimbine is a selective inhibitor of a-2- adrenergic receptors and, while at low dose it has hypertensive activity, at high dose it is hypotensive (vasodilation of peripheral vessels). It is the vasodilation of peripheral vessels, and especially vasodilation of the corpus cavemosum, which is the cause of the reputation of yohimbine as an aphrodisiac (90). Tests have shown, indeed, that increased... 

Chlorpromazine has complex actions on the cardiovascular system, directly affecting the heart and blood vessels and indirectly acting through CNS and autonomic reflexes. Chlorpromazine and less potent antipsychotic agents, as well as reserpine, risperidone, and olanzapine, can cause orthostatic hypotension, usually with rapid development of tolerance. 

Both cardiac output and peripheral vascular resistance are reduced during long-term therapy with reserpine. Orthostatic hypotension may occur but does not usually cause symptoms. Heart rate and renin secretion fall. Salt and water are retained, which commonly results in pseudotolerance. ... 

A review article on certain aspects of the pharmacological properties of most of the iboga alkaloids has appeared (41). Several compounds stimulated the central nervous system in a way which was not amphetamine-like and manifested itself in a number of cases as antagonism against the reserpine catalepsy. Many of the compounds caused hypotension and bradycardia in anesthetized cats. Under these conditions ibogaline was the most active alkaloid. Coronaridine is said to produce a significant diuresis (42) and catharanthine has some hypoglycemic activity (43). 

Reserpine produces sedative, hypotensive, and tranquilizing effects. This is due to its actions of causing depletion of monoamines from presynaptic nerve terminals in central and peripheral nervous systems. The adverse side effects are drowsiness, nightmare, depression, excessive salivation, nausea, diarrhea, increased gastric secretion, abdominal cramps, and hypotension. 

The pharmacological properties of deserpidine are similar to those of reserpine, causing sedation and tranquilization. Toxic effects from high doses include drowsiness, depression, nansea, diarrhea, abdominal cramps, and hypotension. It is less toxic than reserpine. However, the poisoning effects may be greater than those of other Rauwolfia alkaloids, such as rescinnamine. An oral LD50 value in mice is 500 mg/kg. 

Not understood. A possible explanation is that because the rauwolfia alkaloids deplete the neurotransmitter from the sympathetic nerve supply to the heart, the parasympathetic vagal supply (i.e. heart slowing) has full rein. Digitalis also causes bradycardia which in the presence of the rauwolfia becomes excessive. In this situation the rate could become so slow that ectopic foci, which would normally be swamped by a faster, more normal beat, begin to fire, leading to the development of arrhythmias. Syncope could also result from the combination of bradycardia and the hypotensive effects of reserpine. 

The primary actions of reserpine alkaloids are caused by inhibition of noradrenaline and depletion of amines in the central nervous system. While the hypotensive effects have a slow onset their duration is long, and the effective dose is sufficiently low to limit any side effects. It was previously used as a tranquilliser however, the much higher doses required often resulted in depression and Parkinson disease-like symptoms (Huang 1993). As a result Rauwolfia has become a restricted herb in Australia and has no place in current herbal prescribing. 

An advantage of clonidine is the absence of orthostatic hypotension, but like a-methyldopa and reserpine it may cause drowsiness, and marked sedation occurs in up to 50% of patients treated in some series. Sedation can be so severe as to proceed to semi-consciousness. Nightmares and delusions are another expression of the drug s influence upon the central nervous system. Apart from sedation, the complaint of dry mouth and nose is the most common side effect recorded with clonidine administration. Dizziness, headache and fatigue are frequently mentioned, as well as anorexia, nausea, constipation and even pseudo-obstruction (94 ), anxiety, depression, drug fever and rashes. Side effects occur in 50—70% of the patients treated and are in some 20% the reason for discontinuation of therapy (3 , 13, 83 ). 

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