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

To assess if induced hyperinsulinemia enhances blood pressure (BP), three tests were performed to nine healthy volunteers as follows: A. After an oral dextrose load (75 g), 250 ml of 0.9% NaCl plus 25 g dextrose were infused in three hours. B. The same procedure, plus 15 U of regular insulin in the intravenous solution. C. (control) The same procedure but without insulin and dextrose. Pulse and BP were measured every 15 minutes, serum glucose and insulin were determined hourly. Hyperinsulinemia from 2 to 7-fold the basal value was induced in the test A, and from 7 to 30-fold in the test B (P less than 0.01). BP did not rise with hyperinsulinemia, but a slight and nonsignificant decrease of mean BP and higher heart rate (P less than 0.05) were noticed at the third hour in the test B. Acute hyperinsulinemia do not cause high BP. A cause-effect relationship between hyperinsulinemia and hypertension is still unproved.
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PMID:[The effect of acute hyperinsulinemia on arterial pressure in healthy individuals]. 209 27

Soskin, in his 1946 textbook, stated that insulin may be regarded as the dominant instrument in the symphony of endocrine action that results in normal carbohydrate metabolism. After almost half a century, great progress in the medical field has revealed that insulin plays more than even he described. Some aspects of important actions of insulin in our field as investigated in our laboratory are summarized below. 1. Role of insulin in reproductive endocrinology. (1) Correlation of insulin and testosterone in normal young women and patients with polycystic ovary syndrome (PCO). The sum of serum insulin values during 75g OGTT and serum testosterone values were positively correlated in normal women and patients with PCO. Glucose transport activities in isolated adipocytes from a typical PCO patient were decreased, but insulin binding activities were not, which indicates that insulin resistance in this patients is due to some post-receptor defects. (2) Insulin may be a risk factor of endometrial carcinoma. It is well-recognized that several diseases associate with hyperinsulinemia, such as obesity, PCO, diabetes mellitus, and hypertension are risk factors for endometrial carcinoma. The sum of the insulin values during OGTT was significantly higher in patients with endometrial carcinoma than in those without. 2. Role of insulin in perinatal medicine. (1) Increase in insulin secretion during pregnancy. High serum insulin concentration during OGTT, increased secretion of urinary C-peptide, and enhanced staining of insulin in B cells by the PAP method suggest that insulin secretion is enhanced during pregnancy. (2) Insulin resistance during pregnancy. Glucose utilization rate in both pregnant and progesterone-treated rats, as assessed by a glucose clamp technique, is significantly decreased as compared to nonpregnant rats. The technique of 2-deoxyglucose injection revealed that whole body insulin resistance is due to insulin resistance in individual insulin-sensitive tissues. The activities of 3-0-methyl-D-glucose transport in isolated rat skeletal muscle and human adipocytes were found to decrease during late pregnancy, but insulin binding activities were not. These results suggest that insulin resistance during pregnancy is due to some post-receptor mechanisms. (3) Physiological meaning of insulin in fetal growth.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The role of insulin in reproductive endocrinology and perinatal medicine]. 223 Apr 12

1. Regular consumption of 1 g/kg of alcohol for 4 days did not significantly alter mean 24 h blood pressures compared with a similar period when dextrose was consumed to match caloric intake. 2. In contrast, the variability of diastolic blood pressure was increased by regular alcohol consumption. 3. Increased blood pressure variability in response to the stress of blood pressure measurement may contribute to the observed association between hypertension and alcohol consumption.
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PMID:Effects of regular alcohol consumption on 24 hour ambulatory blood pressure recordings. 234 15

The effect of progressive increases in intraluminal glucose concentration on proximal tubule sodium absorption was studied in normal and streptozotocin diabetic rats by microperfusion. Each tubule was perfused twice, with and without glucose added to the perfusion fluid. Net sodium and water absorption were markedly enhanced by 300-500 mg% intraluminal glucose in both normal and diabetic rats. Substituting the transported but nonmetabolized glucose analogue, alpha-methyl D-glucoside for glucose also resulted in marked stimulation of sodium absorption, whereas substituting bicarbonate and acetate for chloride in the perfusion solution inhibited the effect of glucose. These observations suggest that the stimulation of sodium absorption by glucose was mediated by the brush border Na/glucose cotransporter. Sodium concentration and osmolality were found to fall markedly to hypotonic levels when high glucose concentrations were in the perfusion fluid. This luminal hypotonicity may be an important driving force for proximal fluid absorption. In poorly controlled diabetes, high filtered glucose concentrations may lead to enhanced proximal sodium and water absorption, which could in turn contribute to volume expansion, hypertension, and renal hypertrophy.
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PMID:Progressive increases in luminal glucose stimulate proximal sodium absorption in normal and diabetic rats. 236 20

Sprague-Dawley rats received infusions of 55-microns microspheres (groups 1 and 3) or dextrose (groups 2 and 4) into both renal arteries. Groups 1 and 2 rats were studied over 7 mo. In group 1 rats renal embolization increased the mean arterial pressure (group 1, 140 +/- 4 mmHg; group 2, 118 +/- 2 mmHg) without reducing the glomerular filtration rate (GFR; group 1, 4.69 +/- 0.16 ml/min; group 2, 4.57 +/- 0.22 ml/min). Micropuncture studies showed that systemic hypertension was accompanied by an increase in the glomerular capillary pressure of functioning nephrons in group 1 rats. Morphological studies showed that renal embolization caused both glomerular ischemia (group 1, 11.8 +/- 1.9% of glomeruli; group 2, 0.1 +/- 0.1% of glomeruli) and glomerular segmental sclerosis (group 1, 15.0 +/- 1.0% of glomeruli; group 2, 3.3 +/- 0.2% of glomeruli). Groups 3 and 4 rats were studied over 2 mo. Renal embolization again increased the mean arterial pressure without reducing the GFR in group 3 rats. Morphological studies showed that at 2 mo renal embolization caused glomerular ischemia without glomerular segmental sclerosis. These studies show that focal glomerular ischemia can cause systemic and glomerular capillary hypertension in the absence of a reduction in the GFR. They further show that focal glomerular ischemia can cause progressive sclerotic injury in the remaining, nonischemic portion of the glomerular population.
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PMID:Hypertension and progressive glomerular injury caused by focal glomerular ischemia. 238 5

The effects of atrial natriuretic factor (0.025 microgram/kg/min) on isoproterenol-(0.02 microgram/kg/min) and furosemide-(5 mg i.v. bolus) stimulated renin release were studied in seven salt-replete healthy volunteers. Isoproterenol or furosemide were given against a background infusion of 5% D-glucose (placebo day) or atrial natriuretic factor (experimental day). Atrial natriuretic factor abolished the rise in plasma renin activity caused by isoproterenol (p = 0.003) and significantly (p = 0.048) attenuated the rise in plasma renin activity after a bolus injection of furosemide. These results show that a pharmacological dose of atrial natriuretic factor inhibits stimulated renin release in humans. This attenuation is apparent with two heterogenous stimuli, which suggests a nonspecific effect.
Hypertension 1989 Jan
PMID:Atrial natriuretic factor inhibits isoproterenol- and furosemide-stimulated renin release in humans. 252 33

Our previous studies demonstrated that chronic dietary NaCl supplementation is associated with significant increases in plasma atrial natriuretic factor in Wistar-Kyoto (WKY) rats but not in NaCl-sensitive spontaneously hypertensive rats (SHR-S). The current study tested the hypotheses that 1) acute volume-induced atrial natriuretic factor release is impaired in SHR-S compared with control NaCl-resistant SHR (SHR-R) and WKY rats maintained on basal (1%) NaCl diets; 2) dietary NaCl supplementation (8% NaCl for 2 weeks) alters acute volume-dependent atrial natriuretic factor release in these strains; and 3) replacement of the deficiency in circulating atrial natriuretic factor seen in NaCl-supplemented SHR-S can reverse the NaCl-sensitive component of hypertension. SHR-S and control SHR-R and WKY rats were placed on 1% or 8% NaCl diets at age 7 weeks; 2 weeks later, right atrial pressure and plasma atrial natriuretic factor were measured in conscious rats before and after acute volume expansion (7, 20, and 60 ml/kg, 5% dextrose, for 1 minute). The slopes of the right atrial pressure x plasma atrial natriuretic factor linear regression for the SHR-S fed both 1% and 8% NaCl were significantly shallower (p less than 0.01) than those of 1% NaCl-fed SHR-R or WKY rats. Dietary NaCl supplementation did not alter right atrial pressure in any strain and blunted acute volume-induced atrial natriuretic factor release in WKY rats, but not in SHR-S or SHR-R, suggesting the dietary NaCl-induced elevation in plasma atrial natriuretic factor levels in WKY rats may be related to impaired clearance, as well as enhanced release, of the peptide. The plasma levels of exogenous atrial natriuretic factor required to abolish the NaCl-induced pressor effect in SHR-S were 12-fold greater than endogenous plasma atrial natriuretic factor levels in 8% NaCl-fed WKY rats, suggesting that impairment of atrial natriuretic factor release does not play a major role in the pathogenesis of NaCl-sensitive hypertension in SHR-S.
Hypertension 1989 Oct
PMID:Atrial natriuretic factor in NaCl-sensitive and NaCl-resistant spontaneously hypertensive rats. 255 22

Micropuncture studies were performed in Munich Wistar rats made diabetic with streptozotocin and in normal control rats. Diabetic rats received daily ultralente insulin to maintain moderate hyperglycemia (approximately 300 mg/dl). Group 1 diabetic rats studied after routine micropuncture preparation exhibited elevation of the single nephron glomerular filtration rate (SNGFR) due to increases in the glomerular transcapillary hydraulic pressure difference and glomerular plasma flow rate. In group 2 diabetic rats infusion of insulin to achieve acute blood glucose control normalized the glomerular transcapillary pressure gradient while increasing the glomerular ultrafiltration coefficient, so that SNGFR remained elevated. Persistent elevation of SNGFR despite normalization of the transcapillary pressure gradient was also observed in group 3 diabetic rats infused with insulin plus sufficient dextrose to maintain hyperglycemia. These studies indicate that glomerular capillary hypertension in diabetes is an acutely reversible consequence of insulin deficiency and not the result of renal hypertrophy.
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PMID:Control of glomerular hypertension by insulin administration in diabetic rats. 264 14

Hemodynamic and biochemical effects of the new renin inhibitor CGP 38560A (molecular weight 826) were tested in 15 healthy volunteers after a single-blind, randomized, placebo-controlled protocol. At a 2-week interval, groups of five subjects received a 30-minute infusion of either 5% dextrose or CGP 38560A 50, 125, or 250 micrograms/kg. Blood pressure, heart rate, plasma renin activity, active and total renin, angiotensin-(1-8)octapeptide (angiotensin II), and aldosterone were sequentially measured up to 3 hours from the onset of the infusion. There was no consistent change in blood pressure or heart rate. Plasma renin activity and angiotensin II decreased dose dependently, and peak suppression was observed at the end of the infusion of CGP 38560A and after the 250-micrograms/kg dose. Plasma renin activity fell from 1.0 +/- 0.19 (mean +/- SEM) to less than 0.05 ng/ml/hr in all five subjects (p less than 0.001), and angiotensin II fell from 7.7 +/- 1.2 to 2.6 +/- 0.9 femtomole/ml (p less than 0.01). Active renin rose fourfold from 24 +/- 1.9 to 98 +/- 14 pg/ml (p less than 0.001) at the end of the infusion of the high dose. Plasma angiotensin II returned toward its initial values much faster than plasma renin activity and active renin. In conclusion, CGP 38560A was well tolerated. It induced a dose-dependent decrease in angiotensin II and plasma renin activity and a long-lasting and dose-dependent rise in active renin. The doses used did not reduce plasma angiotensin II maximally despite reduction of plasma renin activity to unmeasurable levels.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1989 Jun
PMID:Hemodynamic and biochemical consequences of renin inhibition by infusion of CGP 38560A in normal volunteers. 266 35

A galactose-specific lectin, recently described by our laboratory, is immunologically demonstrable on the surface of neoplastic cells derived from patients with Hodgkin's disease. This Hodgkin's lectin is shown to be functionally and antigenically related to the galactose-N-acetylgalactosamine-specific lectin of the hepatocyte (HBP). Poly- and monoclonal antibodies against either the cytoplasmic tail or the cell-surface binding site of HBP recognize the Hodgkin's lectin as a 55 Kd protein. Expression of the 55 Kd antigen appears to be restricted to Hodgkin's disease involved tissues and cells of the monocyte/macrophage lineage. The putative identification of the Hodgkin's lectin as an ectosialyltransferase unique to Hodgkin's cells is supported by inhibition of enzymatic activity by anti-HBP antibodies. Cultured Hodgkin's cells, in analogy to purified HBP, agglutinate T-lymphocytes mediated by the Hodgkin's lectin. This cell-to-cell interaction results in the incorporation of sialic acid into lymphocyte surface asialoglycans as well as in the stimulation of lymphocyte proliferation. The function of the Hodgkin's lectin as lymphocyte agglutinant in vitro suggests its role as an immunomodulator contributing to the immunodeficiencies associated with Hodgkin's disease.
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PMID:A marker and putative pathoantigen of Hodgkin's cells. 269 Feb 34


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