The effect of arginine vasopressin (AVP) on the gastrointestinal (GI) transit and its possible mechanism were studied using charcoal meal test in mice. A dose related inhibitory effect was recorded. The effect appears to be independent of the time allowed between AVP administration and testing. The studies on the mechanism reveal that AVP acts without involving V1 and V2 vasopressin receptors. An almost complete reversal of the effect by physostigmine and potentiation by atropine indicate that AVP might act through an inhibition of the release of acetylcholine. However, the neural nicotinic receptors mechanisms do not seem to contribute since hexamethonium failed to modify the AVP action. Further, a partial antagonism by naloxone or prazosin pretreatment indicates that opioid and alpha 1 adrenergic systems also contribute to this action of AVP. However, the effect appears to be independent of alpha 2 and beta adrenergic systems since yohimbine and propranolol failed to modify the same.
minipress 6 mg
1. The role of putative neurotransmitters was investigated in morphine-induced Straub reaction (SR) in albino mice. 2. Apomorphine (15 mg/kg) was also effective in inducing SR. However, in a smaller dose (0.2 mg/kg) it blocked SR induced by morphine. 3. Morphine-induced SR was potentiated by tranylcypromine, reserpine (acute effect), imipramine and L-dopa and blocked by reserpine (chronic effect), alpha-methyldopa, pimozide, chlorpromazine, haloperidol and metoclopramide. Prazosin and clonidine partially blocked morphine SR in high doses. 4. Propranolol, yohimbine, cyproheptadine and atropine were ineffective in blocking morphine SR. 5. The results indicate that morphine SR is mediated through release of DA in the CNS which excites central D2 receptors. Activation of central alpha 1-adrenoceptors might also play a minor role.
minipress drug class
A role for parabrachial nucleus in cardiovascular regulation is suggested by evidence that electrical stimulation in this region elicits increase in heart rate and arterial pressure. We hypothesized that parabrachial nucleus may also be involved in control of coronary vasomotor tone. After beta-adrenergic receptor blockade in anesthetized cats, electrical stimulation in the region of parabrachial nucleus produced no change in heart rate, an increase in arterial pressure (34 +/- 6 mmHg), and a transient reduction in coronary blood flow velocity (-21 +/- 2%). Coronary resistance (72 +/- 9%) and femoral resistance (189 +/- 31%) increased markedly. The decrease in coronary blood flow velocity was abolished by stellate ganglionectomy or alpha 1-adrenergic blockade without altering pressor or femoral responses. Injection of the neurotransmitter L-glutamate or kainic acid into parabrachial nucleus also elicited coronary vasoconstriction. We conclude that electrical or chemical activation in the region of parabrachial nucleus elicits coronary vasoconstriction as part of a generalized sympathetic activation. The fact that the coronary response is elicited by chemical activation suggests that cell bodies in the region of medial parabrachial nucleus and subceruleus, as opposed to fibers of passage, are involved in this central neural coronary vasoconstriction.
minipress xl dose
Eight days after coarctation mean aortic pressure proximal to the occlusion was 168(SEM 1.29) mm Hg (n = 104) while distally it was 38(2.42) (n = 40). Of the rings tested 96% showed spontaneous rhythmic activity, having a mean frequency of 3.94(0.17) cycles.min-1. Spontaneous activity was not present in the pressure protected segments taken from the same animals. Rats with the distal kidney removed (n = 25) failed to become hypertensive and similarly prepared ring segments failed to show spontaneous rhythmic activity. Prior removal of the endothelial layer had no effect on the spontaneous contractile responses in pressure loaded segments. Histological examination showed that the media to lumen ratio was increased in coarcted rats in both pressure loaded and pressure protected regions compared to similar regions in sham operated animals.
A rabbit ear model has been developed in which arterial pressure, auricular blood flow conductance, and microvascular perfusion can be followed continuously in conscious animals. Conductance is measured with a transit-time flow probe placed around the auricular artery, arterial pressure is measured with an abdominal aortic catheter, and cutaneous microvascular perfusion is assessed using laser Doppler fluxmetry. Placement of a femoral vein catheter permits administration of vasoactive substances. To date, rabbits have been instrumented for 90 days or longer. Auricular and abdominal arterial pressures were equal, permitting the calculation of auricular artery conductance. Microvascular perfusion as measured by laser Doppler fluxmetry followed changes in overall blood flow. The presence of postsynaptic alpha 2-receptors was confirmed by determining auricular conductance before and after the administration of intravenous alpha-agonists. The development of this unique model will help to advance the understanding of the pathophysiology of human digital thermoregulatory vascular abnormalities.
To compare the efficacy and tolerability of the alpha 1 A-subtype selective drug tamsulosin with the nonsubtype-selective agent alfuzosin in the treatment of patients with lower urinary tract symptoms (LUTS) suggestive of bladder outlet obstruction (BOO), often termed symptomatic benign prostatic hyperplasia (BPH).
minipress max dose
The aim of the present study was to investigate the presence of the immunoreactive oxytocin in human placental extracts and putative factors regulating the release of immunoreactive oxytocin from cultured human placental cells. Fresh placental tissue was collected from pregnant women at term and dissected of membranes (n = 5). Presence of immunoreactive oxytocin in trophoblast tissue was evaluated by a specific radio-immunoassay after acidic extraction and high-pressure liquid chromatography. In a second set of experiments, primary cultures of placental cells were performed and, 48-72 h after dissociation, the effect of arginine vasopressin, corticotropin-releasing factor, neuropeptide Y, activin A, inhibin A, noradrenaline or prostaglandins on immunoreactive oxytocin level in culture medium was investigated. The presence of immunoreactive oxytocin was shown in the acidic extract of trophoblast at term, and in the culture medium of human placental cells, and it was identical to the native peptide. The addition of corticotropin-releasing factor or arginine vasopressin, but not of neuropeptide Y, increased the release of immunoreactive oxytocin three- to fourfold from placental cells, with a dose-dependent effect (P < 0.01). A significantly increased release of immunoreactive oxytocin was shown in presence of noradrenaline (P < 0.01), which was reversed by prazosin, an antagonist of alpha-adrenergic receptors. Recombinant human activin A (P < 0.01), but not inhibin A, stimulated the release of immunoreactive oxytocin three- to fourfold from placental cells. Prostaglandin F2 alpha was a potent secretagogue of immunoreactive oxytocin, whereas a partial or no effect was observed when prostaglandin E2 or prostaglandin I2 was added. Thus, the present findings showed that human placenta contains immunoreactive oxytocin, and that its release from cultured placental cells is regulated by neurohormones, growth factors or prostaglandins.