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)

We compared guanine nucleotide regulatory protein (G protein) levels and function in plasma membranes from resistance vessels (mesenteric arteries) isolated from spontaneously hypertensive (SHR) and normotensive Wistar rats. G protein function was deduced from studies of adenylate cyclase activity. Although the basal level of adenylate cyclase activity (+/- Mn2+ ions) was significantly greater in SHR membranes, addition of agents that function via the stimulatory G protein--i.e., NaF (10(-2) M), (-)-isoproterenol (10(-4) M), and prostaglandin E1 (10(-5) M)--resulted in a significantly lower stimulatory response in SHR membranes. Ligands that function via the inhibitory G protein--i.e., adrenaline (10(-5) M)/propranolol (10(-5) M) (this combination being equivalent to an alpha 2-receptor agonist), carbachol (10(-3) M), and serotonin (10(-5) M)--were responsible for only slight inhibitory responses in both SHR and Wistar rat membranes, which were not significantly different. Western blotting identified the presence of Gs, Gi2, and Gi3 alpha-subunits in rat vascular smooth muscle, but there were no differences in the levels of these G protein alpha-subunits found in SHR and Wistar rat plasma membranes. The levels of the beta-subunit in the two sets of membranes were also similar. In conclusion, there is a reduced response in adenylate cyclase activity to agents that function via the stimulatory G protein in SHR membranes. However, this is not a consequence of altered levels of the different G protein subunits.
Hypertension 1993 Feb
PMID:Guanine nucleotide regulatory proteins in the spontaneously hypertensive rat. 842 82

We have investigated the ability of the one-kidney, one-clip (1K,1C) hypertensive rat to develop a hyperthermic response to intracerebroventricular injection of prostaglandin (PG) E1. Accordingly, core temperature was monitored in response to PGE1 injections both preoperatively and on days 4, 8, 12, and 18 after either unilateral nephrectomy or the induction of hypertension due to nephrectomy plus renal artery clipping. Temperature responses to PGE1 were similar throughout each test day in normotensive, unilaterally nephrectomized control rats. In contrast, 1K,1C rats became hypertensive within 4 days of renal artery clipping, and at this time the hyperthermic response to PGE1 was virtually abolished. A reduced hyperthermic response was also seen at 8 and 12 days after clipping; by 18 days responses were again similar to controls. To determine whether central arginine vasopressin (AVP) was involved in the suppression of the hyperthermic response, we pretreated other hypertensive rats centrally with the V1-AVP antagonist [d(CH2)5Tyr(Me)]AVP before PGE1 injection. In 1K,1C animals thus treated, temperature responses 4-12 days after clipping were indistinguishable from those of similarly treated normotensive control rats. We suggest that the reduced hyperthermic responses to PGE1 seen in the 1K,1C rats during the initial development of hypertension may be due to activation of brain AVP pathways.
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PMID:Suppression by central AVP of prostaglandin E1 hyperthermia in one-kidney, one-clip Goldblatt hypertensive rats. 843 Aug 75

We evaluated the preoperative and intraoperative general condition of 33 pediatric kidney recipients. Eighteen patients were anaesthetized with lumbar epidural anaesthesia. Ten patients were with nitrous oxide-oxygen-halothane, 5 cases were with NLA. Preoperatively many children had cardiovascular and metabolic complications. For example 39% of patients had history of hypertension. Sixty-seven percent of patients were found to have cardiomegaly (cardio-thoracic ratio > 50%) with chest X-ray film. Seven of 9 patients undergoing echocardiogram had abnormality of cardiac wall motion, valvular impairment, pericardial effusion. In forty-eight percent of patients, hyperlipidemia was found. During operation we could not maintain the cardiovascular stability following intratracheal intubation and manipulation of vena cava or abdominal aorta under NLA or nitrous oxide-oxygen-halothane anesthesia. Epidural analgesia inhibited the cardiovascular fluctuation following these surgical stresses. We concluded that epidural analgesia is the best anaesthesia for pediatric renal transplantation and phentolamine or PGE1 are useful to maintain cardiovascular stability and transplanted kidney function.
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PMID:[Anaesthetic management of pediatric renal transplantation for chronic renal failure]. 843 61

Seventy-eight male diabetics with sexual dysfunction were evaluated by a thorough history, general physical, psychological, neurological and urological examinations, routine laboratory tests, and a duplex ultrasound scan with intracavernous injection of prostaglandin E1 (PGE1). The mean patient age was 55.9 years, and the average onset of sexual dysfunction was 10.0 years after the diagnosis of diabetes. Sixty-eight patients (87.2%) had moderate or severe cavernous arterial insufficiency. Older patients and those having a longer duration of diabetes had a higher incidence of cavernous arterial insufficiency. Cigarette smoking, hypertension, and alcohol abuse were also related to cavernous arterial insufficiency. There was no significant difference in cavernous arterial insufficiency between the insulin-dependent and the insulin-nondependent groups. There were significant differences of diameters and peak blood flow velocities of cavernous arteries between 78 diabetic impotent patients and 10 controls. These findings strongly suggest that the cavernous arterial insufficiency is closely related to the diabetic impotence. In addition, the prevalence of cavernous arterial insufficiency increases with age, duration of diabetes, cigarette smoking, hypertension and alcohol abuse, but it is not definitely correlated with the type of diabetes management.
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PMID:Penile blood flow study in diabetic impotence. 850 92

We studied the clinical symptoms in nine children (seven females and two males; mean age 11.6 years) with severe but transient acute secondary erythermalgia. The classical symptoms at presentation were episodic attacks of painful burning hands and feet which felt warm with congested appearance of the feet. Each attack lasted for a mean period of 25 days (range from 6 to 56 days). The blood pressure was elevated in seven patients. Intravenous sodium nitroprusside was effective in ameliorating the symptoms with drop in blood pressure to normal in five patients; pizotifene, labetolol, prostaglandin E1 and hypnotherapy were effective in each of four separate cases. The episodes of acute secondary erythermalgia were transient in all and did not recur after a mean follow up period of 1.6 years. These cases suggest that acute secondary erythermalgia, however transient, is not rare and can be associated with mild to moderate hypertension which may respond to sodium nitroprusside. A greater awareness of this condition is necessary to make an accurate and timely diagnosis and institute appropriate therapy in order to prevent undue complications.
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PMID:Acute secondary erythermalgia and hypertension in children. Erythermalgia Multidisciplinary Study Group. 858 98

We have previously demonstrated a decreased expression of Gi alpha 2 protein in platelets from spontaneously hypertensive rats that was associated with an altered responsiveness of adenylyl cyclase to hormone stimulation and inhibition. In the present studies, we have used platelets from hypertensive patients and examined the hormonal regulation of adenylyl cyclase as well as the levels of G proteins and their modulation by antihypertensive drug therapy. We performed these studies in platelets from four groups of subjects: normotensive subjects (group 1), untreated mildly essential hypertensive patients (group 2), and treated moderately to severely hypertensive patients whose blood pressure was uncontrolled (group 3) or controlled with drug treatment (group 4). GTP gamma S, 5'-(N-ethylcarboxamido)adenosine (NECA), and prostaglandin E1 stimulated adenylyl cyclase activity to a greater extent in hypertensive patients (group 2). This effect was partially corrected (by approximately 50% to 80%) in the patients under antihypertensive drug therapy (groups 3 and 4). In addition, inhibition of adenylyl cyclase mediated by a ring-deleted analogue of atrial natriuretic factor (C-ANF4.23) observed in control normotensive subjects was blunted in hypertensive patients (group 2) and was not corrected in treated patients. Gi alpha levels determined by immunoblotting were in the same range for the four groups, whereas Gi alpha 2 and Gi alpha 3 levels were decreased by 70% and 60%, respectively, in hypertensive patients (group 2) compared with normotensive subjects. Antihypertensive drug therapy (groups 3 and 4) partially restored Gi alpha 2 levels toward normal (group 1) by about 60% and 70%, respectively; however, the reduced Gi alpha 3 levels in group 2 hypertensive patients were not improved in group 3 but were raised toward normal levels in group 4 by about 55%. These results suggest that the altered responsiveness of platelet adenylyl cyclase to hormones in hypertension and the normalization of the response with antihypertensive drug therapy could partly be due to the ability of the latter to modulate Gi alpha protein expression. These effects on platelet function may underlie the beneficial effects of antihypertensive agents on some of the complications of hypertension.
Hypertension 1996 Jul
PMID:Aberrant adenylyl cyclase/cAMP signal transduction and G protein levels in platelets from hypertensive patients improve with antihypertensive drug therapy. 867 69

The influence of insulin on platelets in vitro has not been exhaustively investigated. To clarify whether insulin affects Ca2+ metabolism in platelets directly or through alteration of other systems regulating intracellular Ca2+ homeostasis, we examined the effect of insulin both alone and in combination with prostaglandin E1 on platelet aggregation and Ca2+ metabolism. Incubation of rat platelets with insulin reduced thrombin-induced Ca2+ influx but did not change thrombin-evoked release of Ca2+ from internal stores or the size of internal Ca2+ stores. The interactive effects of insulin with prostaglandin E1 were only additive, and insulin did not augment the effects of prostaglandin E1 on platelet Ca2+ metabolism. In contrast, insulin did not inhibit thrombin-induced platelet aggregation but did augment inhibition of platelet aggregation by prostaglandin E1. Our results suggest that insulin inhibits platelet function by both prostaglandin E1-dependent and -independent mechanisms.
Hypertension 1996 Aug
PMID:Effects of insulin on calcium metabolism and platelet aggregation. 870 83

A fifty-one-year-old man presented with a history, symptoms, and clinical findings typical of a hypothenar hammer syndrome in his dominant hand. A thrombotic obstruction in the distal section of the ulnar artery with multiple downstream occlusions of proper digital arteries were documented angiographically. Coexistence of additional cardiovascular risk factors (smoking-induced polycythemia, obesity, hypercholesterolemia, and hypertension) was identified. Conservative management with intravenous heparin and prostaglandin E1 together with measures directed at controlling the additional risk factors (repeated venesection, immediate smoking cessation, and low-lipid diet) resulted in a striking clinical and angiographic improvement of the digital perfusion, without resort to interventional measures or thrombolysis.
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PMID:Hypothenar hammer syndrome successfully managed with intravenous prostaglandin E1 and heparin and with correction of the thrombogenic risk profile. A case report. 892 62

A 52-year-old male for CABG developed a severe right heart failure, because of the direct injury to the right ventricular wall, after cardiopulmonary bypass. The volume loading therapy could not improve the cardiac function, then we used an infusion of low-dose prostaglandin E1 (0.02-0.04 micrograms.kg-1.min-1) for the acute right heart failure with increased pulmonary vascular resistance. After continuous infusion of this dose, the pulmonary vascular resistance decreased quickly, the right ventricular ejection fraction increased, and the stroke volume index also improved. These hemodynamic changes are the result of the potent vasodilating effect of PGE1, that especially could decrease selectively the pulmonary vascular resistance, and increase the preload of the left ventricle. This dose of PGE1, did not cause a severe systemic hypertension that is a serious complication during vasodilating therapy with any vasoactive drugs. In the present case, we speculated that the low-dose PGE1, is effective to improve the right ventricular function during the acute right heart failure which resulted from the intrinsic right ventricular dysfunction.
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PMID:[Prostaglandin E1 at low-doses improved right ventricular ejection fraction in anesthetic management for CABG]. 893 28

A premature baby had severe hypertension associated with idiopathic arterial calcification of infancy. Despite the fact that there was laboratory evidence of renin-mediated hypertension, the disease was refractory to specific renin antagonist and failed to respond to conventional medical treatment. Prostaglandin E1 (PGE1) infusion (dosage range 0.017-0.068 microgram/kg/min) promptly controlled hypertension on two occasions. The drug was given for a total of 65 days and then stopped after the appearance of severe thrombocytopenia; other side effects included sporadic hyperthermia and irritability. Blood pressure was then stabilized satisfactory by a multiple-antihypertensive regimen. In the light of these findings, we believe that PGE1 infusion is a possible therapeutic alternative for babies with idiopathic arterial calcification complicated by severe hypertension refractory to conventional treatment.
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PMID:Idiopathic arterial calcification of infancy: effectiveness of prostaglandin infusion for treatment of secondary hypertension refractory to conventional therapy: case report. 896 Apr 99


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