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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the present in vivo study was to investigate in anaesthetized rats, the effects of selective adrenergic agonists and antagonists on basal gastric tone and phasic contractions by the use of a volumetric method. L-phenylephrine, an alpha-1 agonist, induced hypertension, bradycardia and a significant gastric relaxation. Clonidine, an alpha-2 agonist, caused hypotension, bradycardia and a significant gastric contraction and a reduction of the amplitude of phasic contractions. Salbutamol, a beta-2 agonist, induced a dose-dependent tachycardia and a significant inhibition of gastric tone whereas prenalterol, a beta-1 agonist, induced tachycardia without any significant influence on gastric basal tone. Yohimbine, an alpha-2 blocker, significantly decreased gastric basal tone and reversed the inhibition of phasic contractions induced by clonidine. Prazocine, a selective alpha-1 blocker, and propranolol, a non-selective beta-blocker, had no significant influence on gastric basal tone or phasic contractions. It is concluded that sympathetic inhibition of basal gastric tone in the rat is mediated by alpha-1 and beta-2 adrenergic receptors. Activation of alpha-2 adrenergic receptors significantly increased basal gastric tone and reduced the amplitude of phasic contractions. A blockade of alpha-2 receptors significantly decreased basal gastric tone and restored the amplitude of phasic contractions.
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PMID:Effects of selective adrenergic agonists and antagonists on gastric tone in the rat. 168 93

This study was designed to compare the clinical efficacy and safety of oral clonidine and oral labetalol in the treatment of severe hypertension in an emergency department setting. Thirty-six patients with severely elevated blood pressure (mean baseline blood pressure 199/132 mm Hg) without acute end-organ dysfunction were treated with either oral labetalol or oral clonidine in a randomized double-blind prospective study. Labetalol was administered as an initial dose of 200 mg, followed by hourly 200 mg doses up to 1,200 mg. Clonidine was administered as an initial dose of 0.2 mg, followed by hourly 0.1 mg doses up to 0.7 mg. Labetalol reduced diastolic blood pressure in 94% of the patients within 6 hours, with a mean reduction in blood pressure of 54/37 mm Hg. Clonidine reduced diastolic blood pressure in 83% of the patients within 6 hours, with a mean reduction in blood pressure of 57/32 mm Hg. The authors conclude that oral labetalol was comparable to clonidine in efficacy, had a similar incidence of side effects, and offered the clinician a useful alternative for the treatment of severe hypertension in an emergency department setting. Further studies are indicated to determine appropriate dosing regimens for oral labetalol in the acute treatment of severe hypertension.
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PMID:Oral labetalol versus oral clonidine in the emergency treatment of severe hypertension. 172 76

Noradrenaline, adrenaline and mean arterial pressure prior to and 3 hours after clonidine administration were evaluated in order to assess a value of single dose of 0.3 mg clonidine in the diagnosis of pheochromocytoma. The study involved 12 patients with pheochromocytoma, 17 patients with arterial hypertension, and 9 patients with borderline hypertension. Seven healthy volunteers served as a control group. It was found that clonidine decreased noradrenaline levels in all healthy subjects and patients with the primary blood hypertension and did not affect noradrenaline levels in patients with pheochromocytoma. Clonidine decreased noradrenaline levels in two patients with normal resting noradrenaline levels. Simultaneously, clonidine decreased noradrenaline levels in two patients with normal resting levels of this catecholamine. The obtained results indicate low specificity of the clonidine test and its value in the diagnosis of pheochromocytoma in patients with normal noradrenaline blood levels.
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PMID:[Test with clonidine for diagnosing pheochromocytoma]. 184 84

The antihypertensive efficacy and side effects of transdermal clonidine (Catapres-TTS) and oral clonidine in equivalent doses on a weight basis were compared under double blind (double dummy) and cross over conditions in 16 outpatients with mild to moderate hypertension. After four weeks of placebo TTS and placebo tablet treatment, the patients were randomly placed into groups for six weeks of active treatment and, after an intervening week of placebo treatment, a second six week treatment period. Transdermal clonidine reduced supine and standing blood pressures (P less than 0.01) and heart rates (P less than 0.05) compared with the values at the end of the placebo periods, while oral clonidine did so to the extent of supine systolic blood pressure (P less than 0.01) and standing heart rate (P less than 0.05), respectively. There were, however, no differences in the values between transdermal and oral clonidine at the end of these six week periods. The plasma clonidine concentration was lower 12 hours after a dose of oral clonidine than after transdermal clonidine (P less than 0.05). The side effects did not differ. Seven patients said afterwards that they preferred the transdermal treatment, two preferred the oral treatment and four could not state any preference. It is concluded that transdermal clonidine is similar in its effect to oral clonidine in mild to moderate hypertension. Transdermal clonidine once a week may increase patients' compliance with antihypertensive treatment.
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PMID:Transdermal and oral clonidine. 193 Sep 16

Clonidine may be administered intrathecally as an adjunct to local anesthetics or accidentally during attempted epidural analgesia. To examine clonidine's acute maternal and fetal effects, the authors injected clonidine (100, 300, 750, 1500 micrograms cumulative dose at 15-min intervals) intrathecally in nine chronically prepared near-term ewes. Unlike intrathecal saline injection, which did not alter any parameters, clonidine altered maternal blood pressure in a biphasic manner (depression at lower doses and return to baseline after the highest dose). Clonidine produced a dose-dependent decrease in maternal and fetal heart rate. After the highest dose, 1500 micrograms, PO2 decreased in both ewe and fetus, accompanied by fetal hypertension and bradycardia. Clonidine increased maternal and fetal serum glucose, but not cortisol. Although clonidine-induced hypoxemia and hyperglycemia occur only in sheep, fetal bradycardia may limit the usefulness of clonidine in large doses (greater than 10 micrograms/kg) in obstetrics. Lower doses, such as may be used to enhance spinal anesthesia, are well tolerated in sheep.
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PMID:Intrathecal clonidine in obstetrics: sheep studies. 196 16

Reports suggested that the predominant site of action for the antihypertensive effects of clonidine is the rostral ventrolateral medulla (RVL), the presumed tonic vasomotor center. This study examined whether clonidine directly interacts with nerve terminal alpha 2-adrenergic receptors in the RVL to inhibit the release of sympathoexcitatory transmitters like glutamate (Glu) and aspartate (Asp), and/or facilitate the release of sympathoinhibitory transmitters like gamma-aminobutyric acid (GABA). Release of GABA and Glu was measured from synaptosomes prepared from the rostral ventral medulla of spontaneously hypertensive rats (SHR), a genetic model of hypertension, and normotensive Wistar-Kyoto rats (WKY). Quantification of neurotransmitter release was performed by high-performance liquid chromatography. Depolarization with 35 mM K+ significantly increased by 58-110% the release of GABA, Glu and Asp; however, no strain differences were observed. In contrast, spontaneous release of GABA and Asp was significantly lower in SHR than that of WKY (-36 and -41%, respectively); this effect was not observed for Glu. Clonidine (1 and 10 microM) enhanced the spontaneous release of GABA (+44%), Asp (+50%) and Glu (+70%) in SHR, but not WKY; this effect was prevented by yohimbine (1 microM). These data, together with previous findings, support the presence of facilitory alpha 2-adrenergic receptors on nerve terminals of GABAergic, glutamatergic and aspartatergic neurons in the rostral ventral medulla. These findings also suggest the existence of another inhibitory transmitter that may mediate the actions of clonidine to decrease sympathetic outflow from the RVL.
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PMID:Evidence for clonidine presynaptically modulating amino acid release in the rostral ventral medulla: role in hypertension. 198 40

Clonidine, an alpha-2 agonist, has traditionally been used to treat hypertension. Recently, it has been found to be a potent analgesic when administered either orally, transdermally or parenterally. This antinociceptive action is mediated at the spinal cord level through presynaptic inhibition of norepinephrine. Clonidine is also a valuable adjunct to anesthesia in a variety of clinical scenarios. In this lesson, the potential uses of clonidine will be elucidated, along with an explanation of its pharmacological and physiological mechanisms of action. Clonidine will be explored as an alternative avenue for providing hemodynamic stability and analgesia without the undersirable side effects often encountered with opioids.
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PMID:AANA journal course. 13. New technologies in anesthesia: update for nurse anesthetists--clonidine: an established drug with futuristic indications. 203 97

1. Clonidine resulted in significant suppression of both noradrenaline (NA) and adrenaline (ADR) in essential hypertensives (EHT) without any false positive findings. That is, every patient who failed to suppress had phaeochromocytoma (PH). 2. The clonidine suppression test (CST) produced minimal suppression of NA in NA-secreting PH (NA-PH) and correctly identified two NA-PH with normal basal plasma NA. 3. In ADR-secreting PH (ADR-PH) the CST did not result in significant suppression of ADR levels, whether elevated or normal basally. 4. The CST proved to be an accurate discriminator of PH from other forms of hypertension.
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PMID:Clonidine suppression test reliably differentiates phaeochromocytoma from essential hypertension. 206 69

Five hundred and fifty-nine hypertensive outpatients with diastolic blood pressure between 95 and 110 mmHg participated in this double-blind, placebo-controlled, multicenter study. Eligible subjects were randomly allocated to receive either clonidine (75 micrograms twice daily) or a placebo. After 4 weeks, 'responders' to treatment (diastolic blood pressure reduced to less than or equal to 90 mmHg or by greater than or equal to 10 mmHg) were kept on monotherapy and checked at 4-weekly intervals for another 3 months. Non-responders were given 15 mg chlorthalidone and were also checked for a further 3 months. At the end of the first month, 54.2% of the subjects were responders to clonidine and 41.5% were responders to the placebo (P less than 0.05 for both groups). Of the remaining patients, 69.0% became responders to clonidine plus chlorthalidone, whereas only 34.7% were responders to placebo plus chlorthalidone (P less than 0.01 for both groups). Withdrawals from the study because of excessive diastolic blood pressure levels were about eight times less frequent among the subjects treated with clonidine, either alone or with chlorthalidone. Dry mouth was twice as frequent in the clonidine-treated patients, but there was no significant difference in the incidence of all side effects or the number of withdrawals from the study because of side effects between the two groups. We conclude that low-dose clonidine is effective in the treatment of mild or moderate hypertension. Clonidine-related side effects are still evident, but the overall tolerance profile for this reduced dosage of the drug appears to be favorable.
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PMID:Low-dose clonidine administration in the treatment of mild or moderate essential hypertension: results from a double-blind placebo-controlled study (Clobass). The Clobass Study Group. 216 88

The current study tested the hypothesis that dietary Ca2+ supplementation reverses the NaCl-sensitive component of hypertension and the associated neurochemical abnormalities in the NaCl-sensitive spontaneously hypertensive rat (SHR-S). Male SHR-S were begun on one of four diets at 8 weeks of age: control (0.75% NaCl/0.68% Ca2+); high NaCl (8.00% NaCl/0.68% Ca2+); high Ca2+ (0.75% NaCl/2.00% Ca2+); and high NaCl/high Ca2+ (8.00% NaCl/2.00% Ca2+). High NaCl SHR-S (X2 weeks) had higher mean arterial pressure (MAP) (161 +/- 4 mm Hg) than controls (149 +/- 3 mm Hg; P less than .05). Supplementation with Ca2+ prevented the rise in MAP in high NaCl rats, but did not alter MAP in controls. The 8% NaCl diet elevated plasma norepinephrine and reduced anterior hypothalamic (AHA) norepinephrine stores and turnover; concomitant Ca2+ supplementation restored both plasma norepinephrine and AHA norepinephrine turnover to normal. Clonidine was microinjected into the AHA of rats maintained on the four diets for 2 weeks to test the hypothesis that dietary Ca2+ supplementation prevents the previously observed NaCl-induced upregulation of alpha 2-adrenoceptors in AHA. Clonidine caused dose-dependent decreases in MAP that were greater in high NaCl rats than in controls. The Ca2+ supplementation prevented the exaggerated depressor response to clonidine in the high NaCl group, but not in the controls. The Ca2+ supplementation had no effect on pretreatment MAP or on MAP responses to clonidine in control NaCl-resistant SHR (SHR-R) or Wistar-Kyoto (WKY) rats. Thus, dietary Ca2+ supplementation prevents the NaCl-induced exacerbation of hypertension and augmented depressor response to clonidine in SHR-S by increasing noradrenergic input to AHA, thereby preventing the upregulation of AHA alpha 2-adrenoceptors.
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PMID:Dietary Ca2+ prevents NaCl-sensitive hypertension in spontaneously hypertensive rats by a sympatholytic mechanism. 217 66


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