Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Subthreshold concentrations of angiotensin II (Ang II) potentiate agonist-induced tone in a variety of blood vessels. We measured in vivo the mesenteric artery diameter and blood flow in 12-week-old normotensive Wistar-Kyoto (WKY) rats (n = 20) and spontaneously hypertensive rats (SHR, n = 20); systemic blood pressure was monitored continuously. Phenylephrine (10 mumol/L) superfused on the exteriorized mesentery reduced arterial diameter from 480 +/- 40 to 256 +/- 18 microns (P < .05) in WKY rats and from 562 +/- 26 to 273 +/- 7 microns (P < .05) in SHR, whereas blood flow was lowered by 77% in WKY rats and 76% in SHR (P < .05 in both strains). Topical superfusion of an angiotensin-converting enzyme inhibitor (perindoprilat, 10 and 100 mumol/L) attenuated the phenylephrine-induced decrease in diameter and blood flow in both strains (P < .05). The Ang II type 1 receptor blocker losartan (10 mumol/L) attenuated the phenylephrine-induced decrease in diameter and blood flow in both strains (P < .05). The relaxing effect of losartan was significantly accentuated by the addition of perindoprilat (10 mumol/L) to the superfusate (P < .05 in both strains). Systemic blood pressure was unaffected by the topical application of phenylephrine (10 mumol/L), perindoprilat (10 or 100 mumol/L), or losartan (10 mumol/L). We conclude that phenylephrine-induced tone impairment by angiotensin-converting enzyme inhibition and Ang II type 1 receptor blockade in vivo probably reflects the role of endogenous Ang II in the potentiation of the adrenergic response during the control of vascular tone. This role is identical in both normotensive and hypertensive rats.
Hypertension 1994 Sep
PMID:Endogenous angiotensin II enhances phenylephrine-induced tone in hypertensive rats. 808 38

Injuries caused by compression of spinal nerve roots are frequently encountered clinically. Experimental studies show that several different factors affect the pathophysiologic changes that occur after these injuries. However, the effect of hypertension in conjunction with graded compression of spinal nerve roots is yet unclear. A previously established porcine model was employed, in which the spinal nerve roots were exposed and compressed by an inflatable balloon. Impulse propagation across the compressed nerve segment was studied by the recording of efferent and afferent nerve action potentials, and nerve conduction velocity. The systemic blood pressure was increased by administration of Neo-Synephrine hydrochloride (phenylephrine HCl) (Winthrop Pharmaceuticals, New York, NY) and elevated 40 +/- 5 mm Hg above the normal (100 +/- 5 mm Hg), and electrophysiologic baseline values were recorded. The spinal nerve roots were then compressed for 2 hours with either 0 (control), 50, 100, or 200 mm Hg. The balloon was deflated and the nerve roots were allowed to recover for 1.5 hours. Impulse propagation was studied every 15 minutes and hypertension was maintained throughout the experiment. The results showed no significant changes of the efferent and afferent nerve action potentials at 0.50 or 100 mm Hg. At 200 mm Hg, efferent and afferent nerve action potentials decreased rapidly and were almost abolished within 20 minutes of compression. Some but not significant recovery was seen of the nerve impulse. Compared to data from normotensive pigs in an earlier experiment, the current study showed that hypertension significantly decreases the susceptibility of the spinal nerve roots to compression at and below 100 mm Hg.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of induced hypertension and acute graded compression on impulse propagation in the spinal nerve roots of the pig. 823 28

Hyperinsulinemia may contribute to the development of hypertension. The aim of the present study was to determine whether hyperinsulinemia modulates vascular reactivity to phenylephrine or angiotensin II. In 10 young, healthy volunteers, the left brachial artery was cannulated for drug infusion and direct measurements of arterial pressure. We measured forearm blood flow by a strain-gauge plethysmograph while infusing phenylephrine (0.2, 0.8, and 2.4 micrograms/min) and angiotensin II (5, 10, and 20 ng/min) locally into the brachial artery before and during simultaneous intra-arterial infusion of insulin (0.15 mU/kg per minute). Forearm vascular resistance was calculated from directly measured arterial pressure and forearm blood flow. Intra-arterial infusion of insulin raised the local plasma insulin level from 10.3 +/- 1.4 to 133.3 +/- 21.1 microU/mL (P < .01) and did not change blood glucose level in the venous effluents of the forearm. Insulin infusion slightly but not significantly increased basal forearm blood flow (4.6 +/- 1.5 to 5.5 +/- 0.9 mL/min per 100 milliliters, NS) and decreased forearm vascular resistance (22.1 +/- 2.1 to 20.3 +/- 2.8 U, NS). Phenylephrine and angiotensin II increased forearm vascular resistance dose dependently before and during simultaneous insulin infusion (P < .01 for both). Intra-arterial infusion of insulin attenuated vascular reactivity to phenylephrine (P < .01) and angiotensin II (P < .01). None of these drugs changed blood pressure or heart rate. Our results suggest that hyperinsulinemia attenuates vascular reactivity in the forearm resistance vessels in healthy humans.
Hypertension 1993 Jul
PMID:Intra-arterial infusion of insulin attenuates vasoreactivity in human forearm. 831 94

The blood-brain barrier minimizes the entry of macromolecules into brain tissue. During acute increases in arterial blood pressure, disruption of the blood-brain barrier occurs primarily in cerebral venules and veins. Mechanisms by which increases in cerebral venous pressure produce disruption of the blood-brain barrier during acute hypertension are not clear. The goal of this study was to determine the role of activation of protein kinase C in disruption of the blood-brain barrier during acute hypertension. We examined the microcirculation of the cerebrum in vivo. Permeability of the blood-brain barrier was quantitated by the formation of venular leaky sites and clearance of fluorescent-labeled albumin (FITC-albumin) before and during phenylephrine-induced acute hypertension. In addition, we examined changes in pial arteriolar and pial venular pressure before and during phenylephrine-induced acute hypertension. We compared responses of the blood-brain barrier to acute hypertension in control (untreated) rats and in rats treated with inhibitors of protein kinase C; calphostin C (0.1 microM) or sphingosine (1.0 microM). Under control conditions, no venular leaky sites were visible and clearance of FITC-albumin was minimal in all groups. Phenylephrine infusion increased systemic arterial, pial arteriolar and pial venular pressures, and increased the formation of venular leaky sites and clearance of FITC-albumin by a similar magnitude in all groups. The findings of the present study suggest that inhibition of protein kinase C does not significantly alter the formation of venular leaky sites and/or clearance of FITC-albumin during acute hypertension. Thus, disruption of the blood-brain barrier during acute hypertension does not appear to be influenced by activation of protein kinase C.
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PMID:Activation of protein kinase C does not participate in disruption of the blood-brain barrier to albumin during acute hypertension. 857 57

The pathogenesis of the hypertension associated with Cushing's syndrome is not completely understood. Sensitivity to pressor agents may play a role. We have investigated this possibility by measuring blood pressure (BP) during incrementally increasing infusions of the alpha-adrenergic agonist phenylephrine. Ten subjects (8 women: 2 men), aged 40 +/- 5 years (mean +/- s.e.m.) with Cushing's syndrome were studied. All had raised BP but none had received any anti-hypertensive treatment for at least 16 days before study. Ten age- (40 +/- 5 years) and sex-matched control subjects were also studied. At 13.30, 30 min after a light meal, subjects had an intravenous cannula inserted, ECG leads and a sphygomanometer cuff attached, and then rested supine in a quiet room for 30 min. Phenylephrine was then infused incrementally at intervals of 5 min. The doses used were 0.3, 0.6, 0.9, 1.35 and 2 micrograms/kg/min. Basal mean blood pressure (MAP) was 108 +/- 2 mm Hg (mean +/- s.e.m.) in patients and 74 +/- 3 mm Hg in controls (P < 0.05) and pulse rate was 75 +/- 5 and 68 +/- 3 beats/min (NS), respectively). MAP increased and pulse rate decreased linearly with time. The rate of rise of MAP was 1.7 +/- 0.4 mm Hg/min in subjects and 1.1 +/- 0.2 mm Hg/min in controls (NS). The rate of decrease of pulse was significantly more rapid in Cushing's subjects than in controls (1.4 +/- 0.2; 0.6 +/- 0.1 beats/min2; P < 0.05). The lack of any increased BP response to alpha-adrenergic stimulation suggests that altered sensitivity is not a major cause of the increased BP seen in patients with Cushing's syndrome.
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PMID:Blood pressure responses to phenylephrine infusions in subjects with Cushing's syndrome. 857 3

The effect of age on basal and stimulated noradrenaline release in the hypothalamic paraventricular nucleus (PVN) of the rat was examined by in vivo microdialysis. Microdialysis probes were inserted into the PVN of 3 and 18 month old anaesthetised Sprague Dawley rats and perfused with a modified Ringer solution. Following four basal 30-min collections, transmitter release was stimulated by perfusion with 100 mM potassium for one collection. After re-equilibration, blood pressure was raised 60 mmHg for 30 min by phenylephrine infusion (1-1.3 mg/kg) then a 2-h recovery period followed. Dialysate collections were injected directly onto a reverse phase HPLC-ECD (HPLC with electrochemical detection). Basal extracellular noradrenaline concentrations were found to be similar in adult and old animals. Basal dihydroxyphenylacetic acid (DOPAC) concentrations were significantly greater in old compared to adult rats (P < 0.05). Potassium depolarisation induced a significant increase in noradrenaline concentrations in both age groups (P < 0.001), however the noradrenaline response to potassium stimulation was significantly reduced in the aged rats (P < 0.05). Potassium-induced decreases in DOPAC and homovanillic acid (HVA) concentrations were seen in both age groups. Following phenylephrine infusion, a modest delayed reduction in noradrenaline levels, which failed to reach statistical significance, was seen. Phenylephrine-induced hypertension was associated with decreased DOPAC and HVA concentrations in adult (P < 0.05) and old (P < 0.05) rats, respectively. These results indicate that ageing is associated with changes in dopaminergic and noradrenergic activity in the PVN of the rat. A reduction in noradrenaline response to maximal stimulation induced by potassium depolarisation was observed with ageing. The alteration in the activity of the catecholaminergic pathways to the PVN induced by phenylephrine infusion appears to be age dependent.
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PMID:Altered in vivo catecholamine release in the hypothalamic paraventricular nucleus of the aged rat. 871 56

Autoregulation and CO2-reactivity can be impaired independently of each other in many brain insults, the so-called 'dissociated vasoparalysis'. The theoretical combination of preserved CO2-reactivity and impaired or abolished autoregulation can have many clinical implications in the daily management of brain injured patients. To optimize their treatment, a bedside assessment of autoregulation and CO2-reactivity is desirable. When cerebral metabolic rate of oxygen is constant, changes in arterio-jugular differences of oxygen (AVDO2) reflect changes in CBF. In these situations relative changes in AVDO2 can be viewed as inverse changes in CBF and used as an evaluation method of CO2-reactivity and autoregulation. In 39 consecutive severe head injury patients with a mean age of 28 +/- 17 years and a diffuse brain injury, cerebrovascular response to changes in pCO2 was tested in the acute phase after injury (18 +/- 8 hours). In 28 of those cases autoregulation was also assessed. A relative CBF value (1/AVDO2) was calculated from baseline AVDO2 and was expressed as 100%. Changes in 1/AVDO2 after inducing pCO2 changes give a good estimate of changes in global CBF. Two different indexes were calculated for CO2-reactivity: 1) absolute CO2-reactivity (CO2RABS) and 2) percentage reactivity (CO2R%). CO2R% was used to separate patients with impaired/abolished CO2-reactivity from those with preserved CO2-reactivity. Patients with CO2R% above 1% were considered in the intact CO2-reactivity group and patients in whom CO2R% was below or equal to 1% were included in the impaired/abolished CO2-reactivity group. Only five cases (12.8%) presented an impaired/abolished CO2-reactivity. AVDO2 response to induced hypertension was studied in a subset of 28 patients. Phenylephrine was used to increase MABP about 25%. All AVDO2 values were corrected for changes in pCO2. Patients with changes in 1/AVDO2 less than or equal to 20% were included in the intact autoregulation group. Patients with estimated CBF changes above 20% were classified as having an impaired autoregulation (impaired/abolished). In 12 patients (43%) autoregulation was intact. In the remaining 16 patients (57%) autoregulation was imparied. Of the 28 cases, CO2-reactivity was impaired in only five cases. All patients with an impaired CO2-reactivity also had an impaired autoregulation. Monitoring relative changes in AVDO2 permits a reliable study of CO2-reactivity and autoregulation at the bedside. Introducing these variables into the day-to-day management should be considered in treatment protocols.
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PMID:Arterio-jugular differences of oxygen (AVDO2) for bedside assessment of CO2-reactivity and autoregulation in the acute phase of severe head injury. 873 94

It is common practice in many ophthalmic units to administer multiple applications of 10% phenylephrine in combination with an anti-cholinergic agent to ensure adequate pupil mydriasis prior to routine cataract surgery. Phenylephrine is a pure alpha-1 adrenoreceptor agonist known to produce marked systemic vasoconstriction and associated hypertension with occasional profound reflex bradycardia. Many reviews have suggested caution in the use of 10% phenylephrine in the elderly or hypertensive patient. In a prospective, randomised trial we have assessed pupil dilation comparing the efficacy of 10% phenylephrine (53 patients) versus 2.5% phenylephrine (62 patients). When administered in conjunction with 1% cyclopentolate four times over 1 hour pre-operatively, 2.5% phenylephrine was found to be as effective as 10% phenylephrine in the initiation and maintenance of mydriasis during both extracapsular and phacoemulsification cataract extraction.
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PMID:A comparative study of the efficacy of 2.5% phenylephrine and 10% phenylephrine in pre-operative mydriasis for routine cataract surgery. 953 65

We examined the role of nitric oxide (NO) in the inherited resistance or susceptibility to hypertension in the Sabra hypertension-prone (SBH) and hypertension-resistant (SBN) rat. Basal mean arterial blood pressure was significantly greater in SBH than in SBN rats. Phenylephrine elevated blood pressure to a similar extent in both substrains, whereas the NO synthase inhibitor NG-monomethyl-L-arginine (L-NMMA) had a greater pressor effect in SBN rats. The vasoconstrictor potency of phenylephrine was significantly higher in endothelium-intact aortic rings from the SBH rat, whereas the vasoconstrictor potency of L-NMMA was higher in those from the SBN substrain. Acetylcholine-induced endothelium-dependent relaxation was greater in aortic rings from SBN rats. The vasodilator potency of glyceryl trinitrate was significantly higher in aortic rings from SBH rats and was enhanced after endothelium removal. Both the activity of calcium-dependent NO synthase from aortic endothelial cells and the basal concentration of nitrite/nitrate in plasma were significantly greater in SBN than in SBH rats. In normotensive Wistar rats, basal mean arterial blood pressure, the pressor effect of L-NMMA, endothelial NO synthase activity, and plasma nitrite/ nitrate concentrations were all between the values in SBH and SBN rats. These results indicate that a decrease in NO generation plays a role in the susceptibility of SBH rats to hypertension. Furthermore, the resistance to hypertension in the SBN strain may be related to increased NO generation.
Hypertension 1996 Sep
PMID:Nitric oxide and the regulation of blood pressure in the hypertension-prone and hypertension-resistant Sabra rat. 879 18

Cellular mechanisms which account for disruption the blood-brain barrier during acute hypertension are not clear. The goal of this study was to determine the role of synthesis/release of bradykinin to activate B2 receptors in disruption of the blood-brain barrier during acute hypertension. Permeability of the blood-brain barrier was quantitated by clearance of fluorescent-labeled dextran before and during phenylephrine-induced acute hypertension in rats treated with vehicle and Hoe-140 (0.1 microM). Phenylephrine infusion increased arterial pressure, arteriolar diameter and clearance of fluorescent dextran by a similar magnitude in both groups. These findings suggest that disruption of the blood-brain barrier during acute hypertension is not related to the synthesis/release of bradykinin to activate B2 receptors.
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PMID:Role of activation of bradykinin B2 receptors in disruption of the blood-brain barrier during acute hypertension. 895 32


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