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

A 21-year-old woman suffering from acromegaly was treated with transsphenoidal subtotal hypophysectomy (microscopy: acidophilic adenoma), followed by x-ray and bromocriptine therapy. Seven years later she was re-operated because of a partial bitemporal loss of vision, intracranial hypertension, and regrowth of the pituitary tumour seen on CT-scan. A large part of the invasive suprasellar tumour was then removed by transcranial approach. The neurosurgery was followed by cobalt radiotherapy and bromocriptine administration. Two years later, symptoms and signs of tumour growth reappeared. Administration of cytostatics, such as doxorubicin (Adriamycin) and lomustine (Belustine), resulted in distinct clinical improvement associated with a seven-fold decrease in the serum growth hormone concentration. The visual field became normal and the intracranial mass on a CT scan decreased markedly. As a result the patient was able to resume work.
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PMID:Cytostatics for acromegaly. Marked improvement in a patient with an invasive pituitary tumour. 368 20

This study investigated the effects of altered extracellular Ca2+ on in vitro femoral arterial smooth muscle responsiveness in deoxycorticosterone acetate (DOCA)-salt hypertensive rats. Compared with controls, femoral arteries from DOCA-salt rats showed a significant increase in sensitivity to KCl and norepinephrine in normal Ca2+ (2.5 mM). Although no difference in maximal contractile response to KCl was observed between groups, there was a significant difference in maximal response to norepinephrine. Dose-response curves in low Ca2+ (0.25 mM) resulted in a significant decrease in the sensitivity of femoral arteries from DOCA-salt rats to KCl and NE so that the responses were similar to those of controls. Relaxation of femoral arteries from DOCA-salt rats after washout of the KCl contraction was significantly slower than that of controls in both low and normal Ca2+. Isoproterenol-induced relaxation of femoral arteries from DOCA-salt rats was significantly attenuated in normal Ca2+. Sensitivity of femoral arteries from DOCA-salt rats to isoproterenol increased in low Ca2+, but maximal relaxation was unaltered. Whereas no difference in maximal relaxation to NaNO2 was seen in femoral arteries from either group in normal Ca2+, a significant decrease in sensitivity to NaNO2 was observed in femoral arteries from DOCA-salt rats. In low Ca2+ the response of femoral arteries from DOCA-salt rats to NaNO2 was similar to that of controls. These results suggest that the increased vascular smooth muscle responsiveness to KCl and norepinephrine seen in DOCA-salt hypertension is due to increased sensitivity of the vascular smooth muscle to Ca2+. Extracellular Ca2+, however, plays only a minor role in the decreased vasodilator responsiveness seen in this form of hypertension.
Hypertension 1986 Jun
PMID:Extracellular calcium and altered vascular responsiveness in the deoxycorticosterone acetate-salt rat. 371 May 58

To investigate mechanisms involved in the high incidence of hypertension in diabetes mellitus, the relationship between renin-angiotensin production and renal prostaglandin E2 synthesis was studied in rats 1 week after diabetes mellitus had been induced by streptozotocin injection. The diabetic rats became hypertensive, although plasma renin activity did not increase despite the plasma volume contraction resulting from polyuria and natriuresis. Subcutaneous insulin injection resulted in a marked increase in plasma renin activity, while more rigid control of diabetes mellitus achieved by constant insulin infusion decreased blood pressure. Cortical renin content and renin release as well as papillary prostaglandin E2 synthesis in vitro were significantly lower in diabetic rats than in nondiabetic controls. Isoproterenol and prostaglandin E2 stimulated renin release in controls, while diabetic rats responded only to isoproterenol. Insulin infusion by pump reversed these abnormalities. An additive effect of a maximum dose of isoproterenol (10(-5) M) and prostaglandin E2 (10(-4) M) on renin release was observed in nondiabetic controls and in diabetic rats treated with insulin pump, but not in untreated diabetic rats. The results suggest that 1) renal renin release and prostaglandin E2 synthesis in diabetes mellitus are insulin dependent, 2) inappropriately lower plasma renin activity in diabetes mellitus may be attributed to a diminished renal renin pool and a lack of renin release in response to renal prostaglandin E2, the synthesis of which is also impaired in diabetes, prostaglandin E2-induced renin release may operate independently from isoproterenol-induced renin release, and impaired renal prostaglandin E2 synthesis may contribute to the development of hypertension in the face of an unchanged prohypertensive renin-angiotensin II system.
Hypertension
PMID:Hypertension in experimental diabetes mellitus. Renin-prostaglandin interaction. 389 14

The role of circulating epinephrine in the regulation of renin release was studied in unanesthetized rats with glucocorticoid-induced hypertension. Biadrenalectomized Wistar rats were made hypertensive with methylprednisolone (20 mg/kg s.c. weekly) for 2 weeks and supplemented with deoxycorticosterone pivalate (10 mg/kg s.c. weekly). Sham-operated controls received the same treatment. Baseline weight, mean intra-arterial blood pressure and heart rate of the groups were the same. In both adrenalectomized and sham-operated rats plasma renin activity was determined after a 30 min infusion of the beta-adrenoceptor stimulant isoproterenol (40 ng/min) or its vehicle. Isoproterenol had no blood pressure effect and accelerated heart rate to a similar extent in rats with and without adrenals. Plasma renin activity was significantly higher in epinephrine-deficient than in sham-operated rats. Renin secretion was significantly enhanced by isoproterenol in both groups of rats. These data therefore indicate that in rats with glucocorticoid-induced hypertension the renin-angiotensin system is activated by adrenalectomy, despite the fact that adrenal insufficiency cannot develop. It also appears that rats lacking of circulating epinephrine for a prolonged period do not exhibit an abnormal responsiveness of renin secretion to the stimulation of renal beta-adrenoceptors.
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PMID:Enhanced renin secretion in adrenalectomized rats with glucocorticoid-induced hypertension. 391 Mar 4

The role of extracellular calcium and high blood pressure stress in altered vascular adrenergic responsiveness in rings of femoral artery from spontaneously hypertensive rats (SHR) was investigated. A model in which partial ligation of the external iliac artery prevents the increase in blood pressure to the ipsilateral femoral artery was used to assess the effect of the increase in pressure stress on these alterations. Age-matched (5-week-old) male Wistar-Kyoto rats (WKY) and SHR were used in the study. Partial ligation was performed before a substantial increase in blood pressure occurred (6 weeks of age), and studies on vascular reactivity were carried out at 10 to 12 weeks of age when the SHR were considered hypertensive (indirect systolic blood pressure greater than 150 mm Hg). Maximal contractility of rings of unprotected femoral artery from the SHR in response to KCl in either a normal (2.5 mM) or low (0.25 mM) calcium Krebs solution was significantly greater (p less than 0.05) than was that of protected vessels from the SHR or protected and unprotected vessels from the WKY; however, no difference in the sensitivity to KCl was observed. Isoproterenol-induced relaxation was significantly attenuated in rings of vascular smooth muscle from unprotected femoral arteries of the SHR (p less than 0.05), while the responses of protected vessels from the SHR were similar to controls. Equilibration of vascular smooth muscle in a low calcium Krebs solution resulted in an increase in beta-adrenergic mediated relaxation in all groups.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension
PMID:Vascular reactivity in the spontaneously hypertensive rat. Effect of high pressure stress and extracellular calcium. 398 69

The effects of sinoaortic baroreceptor denervation (SAD) was studied in left ventricle papillary muscles from rats with 15 days of hypertension, compared to sham operated normotensive controls (SO). SAD muscles develop less force (F) with slower force development (dF/dt) than SO ones, characterizing a depressed contractile performance. To verify if the mechanical response produced by cardiac beta-adrenoceptors stimulation displays a desensitization similar to what is observed for rate changes, percentual changes of F and dF/dt resulting from isoproterenol (IPA) actions were compared in SO and SAD muscles, being similar in both groups. Rest potentiation was analyzed to test if this behavior only occurs during beta-adrenoceptors stimulation or if it is an interference with the contractile machinery. Absolute and percentual changes of F and dF/dt, in SO and SAD rats were again similar, as observed before. The results suggest that in this model of experimental hypertension it is not possible to demonstrate beta-adrenoceptors desensitization in ventricular myocardium. The behavior of SAD muscles must result from changes occurring in a common place for both inotropic interventions probably at the contractile machinery level.
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PMID:Contractile performance of papillary muscles of sinoaortic denervated rats. 408 10

Rats treated with desoxycorticosterone acetate and sodium chloride (DOCA/NaCl) developed a time-dependent increase in blood pressure which was associated with a reduced in vitro beta- and an elevated alpha-adrenergic responsiveness. Isoproterenol-induced relaxation of aortic smooth muscle from the DOCA-NaCl-treated rats was similar to controls 1 week after treatment, was significantly attenuated as the blood pressure began to rise (week 4) and was completely abolished when the blood pressure exceeded 150 mm Hg (week 12). The aortic smooth muscle sensitivity to norepinephrine was significantly increased prior to (week 1), during the rise (week 4) and during the maintenance of an elevated systolic blood pressure (greater than 150 mm Hg; week 12). No significant differences were observed between the two groups in either the contractile response of the aortic ring preparations to potassium chloride or in the relaxation properties in response to sodium nitrite. These results demonstrate that alterations in both the alpha- and beta-adrenergic responsiveness occur in the DOCA/NaCl-treated animal. The enhancement of the alpha-adrenergic responsiveness occurs prior to any change in blood pressure, while the attenuated beta-adrenergic responsiveness parallels the elevation in blood pressure, suggesting that these reciprocal alterations of adrenergic responsiveness may be responsible for the eventual development of hypertension induced with DOCA/NaCl treatment in rats.
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PMID:Time course alterations in vascular adrenergic responsiveness in the DOCA/NaCl-treated rat. 609 Nov 57

In patients with normal-renin, mild (n = 6) or moderate (n = 6) hypertension, the antihypertensive effects of propranolol (80 mg/day) for 1 day or for 2 weeks were evaluated in relation to the degree of beta-adrenoceptor blockade induced. A significant and similar fall in systolic blood pressure was observed after 1 day and 2 weeks on propranolol in both groups of patients. In contrast, diastolic blood pressure showed only a minor decrease after 1 day of therapy (-2 +/- 2 and -3 +/- 1 mm Hg) but a significant drop (-7 +/- 3 and -9 +/- 3 mm Hg) after 2 weeks in the mild and moderate hypertension groups, respectively. Plasma propranolol levels and decreases in resting heart rate and PRA were similar after 1 day and 2 weeks of treatment. Isoprenaline dose-response curves for systolic and diastolic blood pressure, heart rate and PRA showed similar parallel shifts after 1 day and 2 weeks of treatment. The effect of graded bicycle exercise on these parameters were also similarly blunted. These results indicate that over time, systolic blood pressure decreases rapidly whereas diastolic blood pressure shows a delayed fall following initiation of low-dose propranolol therapy, despite the same degree of beta-adrenoceptor blockade.
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PMID:Antihypertensive effect and degree of beta-adrenoceptor blockade after short-term and semi-chronic propranolol therapy. 614 29

The effect of chronic salt treatment on systolic blood pressure and vascular adrenergic responsiveness was studied in rats. Vascular reactivity of aortic smooth muscle to potassium chloride and sodium nitrite was similar in both groups, indicating that salt treatment did not alter the regular contraction and relaxation process of the smooth muscle. Isoproterenol-induced relaxation was similar for both treated and control groups demonstrating that salt treatment had no effect on vascular beta-adrenergic responsiveness. However, when aortic smooth muscle was incubated with angiotensin II or norepinephrine, a significant increase in responsiveness was observed in the aortic smooth muscle of the salt-treated group compared to the control group. Collectively, these results suggest that salt, per se, does not affect systolic blood pressure or peripheral beta-adrenergic responsiveness, but does result in a significantly enhanced alpha-adrenergic responsiveness. The implication of these results for experimental hypertension are discussed.
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PMID:Effects of NaCl on vascular responsiveness in male rats. 614 82

The relaxation of thoracic and abdominal aortae of the spontaneously hypertensive rat (SHR) during prehypertensive (3--5 week old) and hypertensive (12--16 and 22--25 week old) stages was compared to that of matched normotensive Wistar rats (NWRs). In the thoracic aorta, the relaxation response to isoproterenol, acetylcholine, Mg2+, Mn2+, Co2+, and La3+ was less in both prehypertensive and hypertensive SHRs than in the matched NWRs; however, such difference was not evident in the abdominal aorta. Similarly, the relaxing effect of nitroglycerin and papaverine was not different in the aorta preparations of the SHR and NWR. After chronic reserpine treatment of the prehypertensive and hypertensive SHRs, the thoracic aorta still showed less relaxation in response to the aforementioned agents. Isoproterenol, but not other agents tested, produced less relaxation in the thoracic aorta from the renal hypertensive rat than from the control. Our results suggest that the decreased relaxation of the SHR thoracic aorta is not a consequence of hypertension and that the defect in the SHR thoracic aorta cannot be generalized to other vascular beds.
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PMID:Vascular relaxation in the spontaneously hypertensive rat. 616 57


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