Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vasodilator responses to acute intra-arterial infusions of K+ are attenuated in dogs with chronic one-kidney perinephritic hypertension in rats with chronic two-kidney Goldblatt hypertension, and in men with essential hypertension. There is evidence that K+ evokes vasodilation by stimulating vascular smooth muscle membrane Na+-K+-activated adenosine triphosphatase, thereby increasing activity of the cellular Na+-K+ electrogenic pump. We therefore proposed that there may be an underlying decrease in the operation of this pump in vascular smooth muscle of hypertensives. The operation of the cellular Na+-K+ pump may be estimated by measurement of rubidium uptake. Thus, so further investigate our hypothesis, we measured 86Rb uptake in small mesenteric arteries and splanchnic veins from 12 dogs with chronic uncomplicated one-kidney perinephritic hypertension and from 12 normotensive control dogs. Vessels were excised under thiamylal anesthesia and incubated in cold medium (plasma or Krebs-Henseleit solution) for sodium loading and then the velocity of 86Rb uptake was estimated in the absence of or in the presence of ouabain, a specific inhibitor of the Na+-K+ pump. In neither arteries nor veins was there evidence for differences between hypertensives and normotensives in the ouabain-insensitive uptake of 86Rb. In contrast, the ouabain-sensitive 86Rb uptake was depressed by 42% in arteries (P less than 0.05) and by 49% in veins (P less than 0.01) from hypertensive dogs, if incubated in the dog's own plasma. These results indicate that the activity of a ouabain-sensitive Na+-K+ pump may be depressed in vascular tissue from dogs with chronic one-kidney perinephritic hypertension. Because the Na+-K+ pump in vascular smooth muscle is probably electrogenic, such an abnormality, by partially depolarizing the muscle cell membrane, would help to account for the elevated vascular resistance found in these dogs.
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PMID:Depressed function of a ouabain-sensitive sodium-potassium pump in blood vessels from renal hypertensive dogs. 13 55

The cardiovascular responses to acute mental "stress" were compared in the Milan strain of spontaneously hypertensive rats (MHS) and in normotensive control rats (NR). Blood pressure and heart rate were followed in pairs of awake MHS and NR, while defence reactions were provoked by alerting stimuli (noise, vibration). No differences were noted between the two groups in response to "stress" although resting heart rate in MHS was lower than in NR. Administration of atropine or propranolol to MHS and NR showed the MHS to have a higher resting vagal tone and lower sympathetic tone than the NR. Subsequent (at least two weeks later) hemodynamic investigation, under nembutal anesthesia, showed no difference in cardiac output between MHS and NR but a higher stroke volume, presumably related to the lower heart rate in MHS. Thus, total peripheral resistance was increased in MHS as was the ratio left ventricular weight/body weight, and in good proportion to the blood pressure rise. Thus MHS differ substantially in both their responses to "stress" and also hemodynamically from the Okamoto strain of spontaneously hypertensive rat (SHR), being the so far most studied and best known model of essential hypertension in man. In MHS the hypertension is more of a systolic type and is of primarily renal origin. As such, MHS provide another model for investigating the polygenic nature of hypertension in man.
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PMID:Cardiovascular control in the Milan strain of spontaneously hypertensive rat (MHS) at "rest" and during acute mental "stress". 55 79

The haemodynamic shifts during head up and head down tilt were investigated in adult spontaneously hypertensive rats (SHR) and matched normotensive control rats (NCR) under nembutal anaesthesia and autonomic blockage. During head up tilt a greater fall in blood pressure and stroke volume was observed in SHR than in NCR, while the reverse was true when tilted in the opposite direction. This altered cardiac response to venous filling, also observed in patients with essential hypertension, is suggested to be caused by an altered Frank-Starling relationship of the hypertrophied heart in hypertensive individuals.
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PMID:Haemodynamic changes during tilt after autonomic blockade in spontaneously hypertensive rats. 60 71

This study was undertaken to define certain differences in cardiovascular function between mongrel (M) and greyhound (GH) dogs. In unanesthetized, trained, chronically instrumented animals mean arterial pressure was significantly higher in the GH (118 vs. 98 mmHg). This was associated with a significantly higher cardiac index in the GH (4.3 vs 3.1 liters/min per m2) and a lower calculated peripheral resistance. Central venous renin activity was significantly lower in the GH when unanesthetized (1.51 vs. 2.88 ng/ml per h). Values of vascular impedance at several selected arterial sites were lower in the GH compared to the M, suggesting differences in arterial wall mechanical properties. The hydraulic power delivered to the aorta by the left ventricle in the GH was twice that of the M (1,166 vs. 564 mol wt). Oscillatory power represented a greater fraction of total aortic power in the GH (15.7 vs. 10.8%). Differences were also observed in the hemodynamic response to acute pentobarbital anesthesia. Thus the young adult GH is hemodynamically different from its mongrel counterpart. These differences bear some resemblance to hemodynamic changes seen in various types of experimental hypertension in animals and to those observed in the early phase of essential hypertension in man.
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PMID:Comparison of arterial hemodynamics in the mongrel dog and the racing greyhound. 125 5

Acute postoperative hypertension (APH) has been documented in the PACU. Over half of the patients who exhibit APH have pre-existing primary hypertension. Sustained blood pressure (BP) elevation increases the risk of myocardial ischemia, infarction, surgical site bleeding, or cerebral hemorrhage in these patients. Following surgery and anesthesia, increased sympathetic stimulation caused by a high level of circulating catecholamines can lead to APH. Some direct perioperative stimulants include pain, anxiety, hypoxia, hypercapnia, hypothermia, shivering, volume overload, and bladder distension. Nursing interventions are directed toward identifying and relieving the cause of APH. Antihypertensive drug therapy with vasodilators or adrenergic inhibitors is used if initial nursing interventions are not effective. Vasodilators frequently used are hydralazine, sodium nitroprusside, and nitroglycerin. Nicardipine has recently been introduced as an intravenous calcium channel blocker. Vasodilators are effective in BP reduction but may cause reflex tachycardia when used alone. Adrenergic inhibitors, such as esmolol and labetalol, block alpha and/or beta receptors to decrease heart rate and BP. Labetalol's effectiveness, relative freedom from side effects, and ease of administration have made it a useful drug in the treatment of APH.
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PMID:Acute postoperative hypertension in the hypertensive patient. 173 70

Radiotracer measures of norepinephrine overflow to plasma are well suited for studying both human sympathetic nervous system responses to mental stress and sympathetic nervous pathophysiology in human hypertension. With an experimental laboratory stressor (cognitive challenge), we noted a preferential activation of the cardiac sympathetic outflow; however, in fainting reactions ("vasovagal syncope"), which occur infrequently during the course of central venous catheter placement under local anesthesia, the converse was seen--an almost total withdrawal of cardiac sympathetic activity. In primary human hypertension (particularly in younger patients), a differentiated activation of the sympathetic outflow to the heart and kidneys is present, based on measurements of norepinephrine spillover to plasma. It is uncertain whether this is attributable to behavioral factors and represents a component of the defense reaction. We previously reported overflow of norepinephrine into the cerebrovascular circulation (with high internal jugular venous sampling) in humans. Because this is resistant to ganglion blockade, brain neurons--not the cerebrovascular sympathetics--are the presumed source. In a preliminary study, we found higher rates of norepinephrine spillover into the cerebrovascular circulation in patients with essential hypertension than in healthy subjects, suggesting that an underlying increase in central nervous system norepinephrine turnover may be the basis for the increased sympathetic outflow.
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PMID:Biochemical evidence of sympathetic hyperactivity in human hypertension. 201 90

Dental management of 162 cases of medically compromised patients was reviewed. Over the past 3 years and 2 months, 130 patients with certain medical problems underwent 162 cases of dental treatment under local anesthesia. In the present study, research was done chiefly on intraoperative management of these patients. The following results were obtained: 1) In the population of 130 patients, those in their 7th decade were the most numerous. Among the subjects, essential hypertension was the most common underlying disease, and the majority of the patients had accompanying cardio-vascular diseases. 2) When the pre- and post-65-year-old patient groups were compared, the latter group had a higher frequency of multiple medical problems. 3) It is suggested that, to manage patients having hypertension or ischemic heart diseases as a complication, continuous blood pressure measurement and ECG monitoring are essential. 4) Among several local anesthetics, 3% prilocaine with 0.03 U/ml felypressin was used most frequently, especially for those with cardiovascular diseases. 5) In the management of hypertensive and ischemic heart patients, nitrous oxide inhalation sedation was effective. 6) For those who required vasodilation, administration of nifedipine or nitroglycerin was effective. 7) Although one case of syncope and another in which dental treatment procedure had to be suspended were found, no severe complications were encountered.
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PMID:[Dental management of the medically compromised patient. A study of 162 cases]. 215 3

In this study, peripheral circulatory responses during dental treatment under local anesthesia were observed. Changes in hemodynamics data, ECG, systolic blood pressure (SBP), diastolic blood pressure (DBP), digital and ear-lobe plethysmogram (PT), and radials and external carotid artery ultrasonic doppler blood flow (FW) were recorded by means of a multipurpose monitoring system. An improved fixed probe was devised for the purpose of stabilizing the external carotid artery FW record, and the ear-piece facebow system (Hanau, No. 153) was remodeled. Radial FW index D/S1 and external carotid FW index d/S1 were analyzed to determine systolic velocity S1 and diastolic velocity D or d. Pressure tests and cold stimulation tests were performed as fundamental research. Comparative investigations were made of changes in PT and FW in the light of SBP, DBP and heart rate (HR). A total of 71 instances of dental treatment was performed on 25 non-hypertensive patients (N-HT) and 25 patients with essential hypertension (HT). The patients were divided into 2 groups according to the local anesthetic employed: the E group, to whom 1:80,000 epinephrine with an addition of 2% lidocaine was administered, and the NE group, to whom 1:25,000 norepinephrine was administered. Results and conclusions 1. When peripheral blood flow was interrupted during the pressure test, digital PT and radial FW were disappeared. 2. Digital PT, radial diastolic FW D, and index D/S1 decreased greatly as a result of the cold stimulation test. It was suggested that changes in digital PT accord with the diastolic velocity D of radial FW. 3. At the stage of local anesthesia, SBP rose most in the HT-NE group. There was a tendency for digital PT and radial FW D either to decrease or to increase. It was assumed that cardio-stroke volume increased when PT and FW increased. Decreases in digital PT and radial FW apparently indicate increased capillary resistance. 4. Greatest increases in HR at the stage of local anesthesia occurred in the N-HT-E group. Digital PT and radial FW D tended to decrease. In cases of increased HR, PT and FW tended to decrease. In comparison with conditions immediately before treatment, digital PT and radial FW D decreased more in the N-HT group than in the HT group.
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PMID:[Peripheral circulatory responses during dental treatment under local anesthesia. Comparison between plethysmogram and ultrasonic Doppler blood flow]. 262 88

The effects of the rapid infusion of large doses of dibutyryl cyclic AMP (DBcAMP) were studied to clarify the clinical usefulness of its vasodilating action in 32 middle-aged patients, who underwent various types of surgery and developed systolic hypertension of over 160 mmHg during general anaesthesia. DBcAMP was given i.v. with an infusion pump at a rate of 0.6 mg kg-1 min-1 for 20 min. In all patients just after the infusion, systolic arterial pressure decreased from 174.0 +/- 20.7 to 129.0 +/- 23.9 mmHg, diastolic pressure decreased from 93.1 +/- 13.4 to 64.8 +/- 13.3 mmHg, heart rate increased from 81.2 +/- 15.7 to 91.5 +/- 19.5 beats min-1, and urine volume increased from 69.4 +/- 54.8 to 182.7 +/- 143.5 ml h-1. In three patients, cardiac index increased from 3.44 to 4.24 l min-1 m-2. In seven patients, tachycardia exceeding 120 beats min-1 developed. DBcAMP was also effective in patients with a history of hypertension. The strongest antihypertensive effect was observed in patients anaesthetized with nitrous oxide-oxygen and enflurane. We speculate that DBcAMP is useful to control hypertension and may be particularly indicated in patients with cardiac failure, renal disorders and essential hypertension.
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PMID:The control of hypertension with dibutyryl cyclic AMP. 303 96

Forty-two spontaneously hypertensive rats (SHR) and 42 normotensive Wistar-Kyoto rats (WKY) were anesthetized with either halothane or enflurane. Blood pressure, heart rate, cardiac output, distribution of blood flow, plasma renin activity, and plasma catecholamines were measured to determine in what manner the hypertensive animal responded to these two anesthetics. Major findings of the study were that plasma renin activity did not increase in the SHR despite a 25% reduction in MAP. The infusion of saralasin, an angiotensin II antagonist, resulted in a further decrease in blood pressure in SHR anesthetized with halothane but not with enflurane. Plasma catecholamine concentrations were elevated in the awake SHR and were decreased in SHR anesthetized with enflurane. Both halothane and enflurane anesthesia resulted in similar alterations in blood flow in the SHR. The normotensive WKY responded to halothane and enflurane in a different manner than the SHR. Plasma renin activity increased with the decrease in blood pressure with both agents. A further decrease in blood pressure occurred with saralasin infusion in WKY anesthetized with halothane or enflurane. Significant blood flow alterations occurred in the WKY anesthetized with both agents, but enflurane caused the greatest changes. The SHR may prove useful in examining the effects of anesthetic agents and other drugs so that we may have a better understanding of the perioperative management of the patients with essential hypertension.
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PMID:Hormonal and hemodynamic responses to halothane and enflurane in spontaneously hypertensive rats. 388 21


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