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

Contrasting results have been reported regarding the prevalence of hypertension in insulin-dependent diabetes mellitus (IDDM), showing a slightly higher or normal percentage of IDDM patients with elevated blood pressure levels than in the general population. Most of the cross-sectional and prospective studies on the prevalence of hypertension in IDDM show an association between microalbuminuria and elevated blood pressure levels. However, it is not clear whether hypertension is simply secondary to kidney damage or whether hypertension occurs with or even before the development of impaired kidney function. Patients with IDDM have a higher exchangeable body Na+ pool. Na+ retention in IDDM is accounted for by several metabolic and hormonal abnormalities such as hyperglycemia, hyperketonemia, hyperinsulinemia, altered secretion, and resistance to atrial natriuretic peptide. High blood pressure appears to be dependent, at least at some phase, on expansion of extracellular fluid volume as a consequence of defects in the renal secretion of Na+ and water. On the other hand, a tendency toward Na+ retention characterizes all patients with IDDM, whereas hypertension develops only in a subgroup of diabetic patients. One possible explanation for these findings is that a genetic predisposition plays a role in creating susceptibility to hypertension and perhaps to diabetic nephropathy independent of diabetes, even if Na+ retention can further deteriorate this susceptibility to hypertension. With regard to this issue, it has recently been suggested that the risk of kidney disease in patients with IDDM is associated with a genetic predisposition to hypertension. Furthermore, diabetic nephropathy occurs in familial clusters, because diabetic siblings of nephropathic diabetic patients show a higher frequency of diabetic nephropathy than the diabetic siblings of nonnephropathic diabetic patients. One of the possible genetic markers that could be useful to identify the diabetic patients with susceptibility to hypertension and diabetic nephropathy is the Na+(-)Li+ countertransport activity in erythrocytes.
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PMID:Insulin-dependent diabetes mellitus and hypertension. 204 36

To elucidate the contributions of renal, humoral, and arterial baroreceptor reflex components to salt-induced hypertension, we administered 10% NaCl intravenously for 10 days to sinoaortic-denervated rabbits with unilateral nephrectomy (n = 7), sinoaortic-denervated rabbits with intact kidneys (n = 7), and sham-operated sinoaortic-denervated rabbits with unilateral nephrectomy (n = 7). Serial changes in mean arterial pressure (MAP), heart rate, and blood pressure variability were recorded. In sinoaortic-denervated rabbits with unilateral nephrectomy, MAP increased significantly from 109 +/- 2 to 124 +/- 3 mm Hg (day 4) and remained elevated for the rest of the experiment. This elevation of MAP was accompanied by a reduction in the standard deviation of MAP, with significant elevations in plasma vasopressin, norepinephrine, and atrial natriuretic peptide concentrations and in sodium retention. In the other groups, there were no significant changes in these vasoactive hormones. In the sham-operated sinoaortic-denervated rabbits with unilateral nephrectomy, sodium retention was similar to that of sinoaortic-denervated rabbits with unilateral nephrectomy. Continuous infusion (1 microgram/kg/hr) of a V1 antagonist prevented the elevation of blood pressure and plasma norepinephrine, the accumulation of sodium, and the reduction of blood pressure lability, whereas a bolus injection (10 micrograms/kg) on day 4 reduced blood pressure from 128 +/- 3 to 115 +/- 2 mm Hg (p less than 0.005). These results imply that vasopressin plays a crucial role in the expression of salt-induced hypertension in rabbits with compromised baroreceptor and renal function.
Hypertension 1991 Jun
PMID:Role of vasopressin in salt-induced hypertension in baroreceptor-denervated uninephrectomized rabbits. 204 53

To elucidate the expression of the brain natriuretic peptide gene in the human heart, we have measured brain natriuretic peptide mRNA levels in hearts using the Northern blot hybridization method. Brain natriuretic peptide mRNA was present with a size of approximately 0.9 kb in the ventricle as well as in the atrium. The brain natriuretic peptide mRNA level in the ventricle was 52% of that in the atrium, whereas the atrial natriuretic peptide mRNA level in the ventricle was approximately two orders of magnitude lower than that in the atrium. Taking atrial and ventricular weights into account, the total amount of brain natriuretic peptide mRNA in the ventricle represented 77% of that in the whole heart. These results demonstrate that most of brain natriuretic peptide mRNA occurs in the ventricle, in contrast with atrial natriuretic peptide mRNA, which is present mainly in the atrium, indicating that the ventricle is a major production site of brain natriuretic peptide.
Hypertension 1991 Jun
PMID:Expression of brain natriuretic peptide gene in human heart. Production in the ventricle. 204 61

Studies of normotensive offspring of hypertensive parents offer the potential to identify inherited abnormalities that contribute to essential hypertension. We compared renal and systemic hemodynamic responses to saline infusion between normotensive sons of two hypertensive parents (SOHT) and sons of two normotensive parents (SONT) selected from the general population of Rochester, Minn. Hemodynamic measurements were performed after a week of low sodium intake (10 meq/day) and were repeated after a week of high sodium intake (200 meq/day). Despite being in the normotensive range, blood pressures in SOHT were higher than those in SONT during low sodium (124 +/- 3/85 +/- 3 versus 118 +/- 2/71 +/- 2 mm Hg, p less than 0.01) and high sodium (122 +/- 3/80 +/- 3 versus 112 +/- 2/70 +/- 2 mm Hg, p less than 0.05) conditions. Higher pressures in SOHT were associated with elevated systemic and renal vascular resistance. After a high sodium diet, renal vascular resistance in SOHT rose further during acute saline infusion, whereas systemic vascular resistance did not change. After a low sodium diet, this renal vasoconstrictor response to saline infusion in SOHT was not present, and renal vascular resistance fell to levels not different from SONT. Plasma renin activity, aldosterone, and atrial natriuretic peptide did not differ between SONT and SOHT. Circulating levels of norepinephrine were higher in SOHT. These data demonstrate a renal vasoconstrictor response to saline infusion in normotensive SOHT, which depends on prior sodium intake. This alteration in renal hemodynamics may represent an inherited abnormality related to the development of hypertension.
Hypertension 1991 Jun
PMID:Renal vascular response to sodium loading in sons of hypertensive parents. 204 80

We assessed the changes in atrial natriuretic peptide (ANP) and its messenger RNA (mRNA) levels in atria and ventricles in relation to hemodynamic factors during antihypertensive treatments in two-kidney, one-clip renovascular hypertensive rats (RHRs). Hypertension of 10-week duration caused a twofold increase in the left ventricular weight/body weight ratio, a significant increase in left ventricular end-diastolic pressure, and an eightfold increase in left ventricular ANP mRNA levels in RHRs, as compared with the levels in control rats. Uninephrectomy or 4 weeks of treatment with the converting enzyme inhibitor enalapril reduced the blood pressure to the control level, with the complete reversal of left ventricular hypertrophy, left ventricular end-diastolic pressure, and ANP mRNA levels. Four weeks of treatment with the arterial vasodilator hydralazine significantly, but not completely, reduced the high blood pressure, but it did not influence left ventricular hypertrophy, end-diastolic pressure, and ANP mRNA levels. The increased ANP synthesis observed in the right ventricles of RHRs also reverted to the control level by uninephrectomy or enalapril treatment, but not by hydralazine, with a time course similar to that of left ventricular ANP. In addition, uninephrectomy caused the left and right ventricular ANP and ANP mRNA levels of RHRs to fall to the levels of control rats as early as 1 week, despite persistent left ventricular hypertrophy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes of atrial natriuretic peptide and its messenger RNA with development and regression of cardiac hypertrophy in renovascular hypertensive rats. 213 12

Neuronal and glial cultures from the hypothalamic-brain stem areas of 1-day-old normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive (SH) rat brains stained positively with atrial natriuretic peptide (ANP)-specific antibodies. The endogenous levels of the ANP immunoreactivity in WKY neuronal and glial cultures were 17.0 +/- 2.2 and 14.3 +/- 2.7 pg/mg, respectively. Comparable neuronal and glial cultures from SH rat brains contained a 48 to 70% decrease in the endogenous ANP immunoreactivity levels. Culture media from both brain cell types also contained ANP immunoreactivity, the levels of which are significantly higher than those found in the cells. However, similar to endogenous levels, the media levels of immunoreactive ANP in SH neuronal and glial cultures were significantly reduced compared with WKY brain cultures. These observations demonstrate that endogenous ANP-like immunoreactivity is found in neuronal and glial cells and is released into the media. The levels of peptide are reduced in cultures of SH compared with WKY cultures, suggesting a genetically controlled difference between the hypertensive and normotensive rat strains long before hypertension develops.
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PMID:Immunoreactive atrial natriuretic peptide in neuronal and glial cells of spontaneously hypertensive rat brain. 213 92

To study the effects of atrial natriuretic peptide (ANP) on body fluid volume regulation, we estimated the changes in intra- and extravascular fluid volume by measuring hematocrit (Hct), plasma protein concentration and water balance, and the changes in intra- and extracellular fluid volume by the electrical impedance method during intravenous infusion of ANP. We did two studies, as follows: ANP was infused into 18 patients with essential hypertension, 29 with renal parenchymal hypertension and 15 normotensives at 0.025 microgram/kg/min for 40 min. Both hypertensive groups showed greater natriuretic responses to ANP than normotensives. ANP infusion into essential hypertensive patients increased the urinary excretion of water by 125%, Na by 205%, Hct by 4.2% and plasma total protein (TP) by 5.2% (each P less than .001). In 9 patients (1 with renal hypertension and 8 normotensives) who did not show a natriuretic response (-2.1%), the infusion of ANP also significantly increased Hct (3.8%) and plasma TP (3.1%, each P less than .01). The electrical impedance method was applied to 12 subjects to simultaneously detect the intracellular (Ri) and extracellular resistivities (Re), of which reciprocals reflect the fluid volume in the extra- and intracellular spaces, respectively. ANP infusion increased Re in all subjects (3.96 +/- 0.16 [SE] v 4.03 +/- 0.16 omega.m, P less than .05), but decreased Ri in 7. Changes in urinary Na excretion correlated positively with those in both Re (r = 0.62, P less than .05) and Ri (r = 0.75, P less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The extrarenal effects of atrial natriuretic peptide on body fluid distribution. 213 3

Because insulin shows an antinatriuretic effect in healthy humans, insulin therapy resulting in circulating hyperinsulinemia may lead to sodium retention and in turn to hypertension in individuals with insulin-dependent diabetes mellitus (IDDM). Moreover, it has been proved that atrial natriuretic peptide (ANP) plays a major role in modulating natriuresis in humans. This study investigated the relationship between insulin and ANP in modulating sodium metabolism in normotensive and hypertensive IDDM subjects compared with control groups of normotensive and hypertensive nondiabetic subjects. IDDM normotensive and hypertensive subjects had mean +/- SE duration of IDDM of 7 +/- 2 and 8 +/- 2 yr, respectively, and had no clinical features of diabetic nephropathy. All subjects received a saline infusion (2 mmol.kg-1.90 min-1) during euglycemia. IDDM normotensive and hypertensive subjects received a subcutaneous insulin infusion (15 mU.kg-1.h-1), resulting in twofold higher plasma free-insulin levels (16 +/- 2 and 19 +/- 3 microU/ml, respectively) than in nondiabetic normotensive and hypertensive subjects (7 +/- 2 and 8 +/- 2 microU/ml, respectively). During saline challenge, sodium excretion increased by 22 +/- 4% in normotensive and 49 +/- 9% in hypertensive nondiabetic subjects but by only 11 +/- 0.4% in normotensive (P less than 0.01) and 8 +/- 2% in hypertensive (P less than 0.01) IDDM subjects. The impaired natriuretic response to saline challenge was mainly due to greater rates of sodium reabsorption by kidney proximal tubules in IDDM than nondiabetic subjects. At baseline, plasma ANP concentrations were significantly higher in both IDDM groups than in control groups (normotensive IDDM and control subjects: 38 +/- 4 and 19 +/- 2 pg/ml, respectively, P less than 0.01; hypertensive IDDM and control subjects: 45 +/- 6 and 27 +/- 4 pg/ml, respectively, P less than 0.05). After saline challenge, ANP concentrations rose to 39 +/- 4 pg/ml in normotensive and 49 +/- 5 pg/ml in hypertensive control subjects, whereas no significant change above baseline value was seen in IDDM subjects. Both IDDM groups showed a 10-12% greater exchangeable Na+ pool than control subjects regardless of the presence of hypertension. Subcutaneous insulin infusion, resulting in circulating plasma free-insulin levels in normotensive control subjects comparable to those in IDDM patients, inhibited natriuresis, increased proximal tubule sodium reabsorption at the level of the kidney, and inhibited an adequate ANP stimulation by saline challenge. We conclude that hyperinsulinemia leads to increased proximal tubule sodium reabsorption and impaired ANP response during saline administration. Both mechanisms account for sodium retention in normotensive and hypertensive IDDM patients.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Role of insulin and atrial natriuretic peptide in sodium retention in insulin-treated IDDM patients during isotonic volume expansion. 213 1

In previous studies, a pharmacological dose of human atrial natriuretic peptide (hANP) was found to increase serum insulin without influencing C-peptide levels. To examine whether blood glucose and insulin response to an oral or i.v. glucose load are influenced by raising hANP levels into the pathophysiological range, eight healthy, normal-weighted, male volunteers were studied. According to a randomized, double-blind study design, an oral glucose tolerance test (ogtt, 75 g) or an i.v. glucose tolerance test (ivgtt, 0.5 g/kg b.w.) were carried out. Beginning 30 minutes before glucose administration infusions of hANP 0.3 micrograms/min) or placebo were given for 180 minutes (ogtt) or 120 minutes (ivgtt). During the hANP-infusions maximal hANP levels were 72 +/- 11 pg/ml (normal less than 25 pg/ml). Responses of blood glucose and C-peptide levels to the glucose load remained unaffected by hANP in both studies. However, hANP increased mean insulin responses (given as area under the curve) by 11.5% in ogtt and by 15.9% in ivgtt (both p less than 0.05). Thus, elevated hANP levels within the pathophysiological range, as observed in chronic heart failure or in hypertension, lead to an increase in serum insulin. Unchanged C-peptide levels demonstrate that hANP does not interfere with insulin secretion, but exclusively inhibits insulin degradation in liver and/or kidney. Further studies are required to elucidate whether these findings play a part in the pathomechanisms of insulin resistance in patients with elevated hANP levels, e.g. in chronic heart failure or hypertension.
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PMID:[The effect of atrial natriuretic peptide on glucose tolerance and insulin level]. 213 3

1. The regional haemodynamic effects of bolus doses (4 and 40 pmol) and infusions (12 and 120 pmol h-1) of endothelin-1 and endothelin-3 were assessed in conscious, Long Evans and Brattleboro (i.e. vasopressin-deficient) rats, chronically-instrumented with pulsed Doppler flow probes. 2. In both strains of rat the lower bolus dose of endothelin-1 caused only a slight pressor effect, but there were marked renal and mesenteric vasoconstrictions and hindquarters vasodilatation. 3. The lower bolus dose of endothelin-3 did not affect blood pressure significantly, although the changes in regional haemodynamics were qualitatively similar to those seen following endothelin-1 in Long Evans and Brattleboro rats. 4. The higher dose of endothelin-1 caused an initial hypotension accompanied by substantial hindquarters vasodilatations in Long Evans and Brattleboro rats. Subsequently, in both strains, there was a rise in blood pressure accompanied by renal, mesenteric and hindquarters vasoconstrictions. 5. The higher bolus dose of endothelin-3 caused initial hypotension and hindquarters vasodilatation similar to those seen with endothelin-1. However, the subsequent pressor effect was less with endothelin-3, as was the renal vasoconstriction, and it did not cause any increase in hindquarters vascular resistance. 6. Infusion of endothelin-1 at the lower rate (12 pmol h-1) caused renal and mesenteric vasoconstrictions in both strains of rat, whereas endothelin-3 at this rate caused only mesenteric vasoconstriction. 7. Infusion of endothelin-1 at the higher rate (120 pmol h-1) caused progressive hypertension and vasoconstrictions in all three vascular beds studied; these were similar in both strains of rat. Endothelin-3 had a smaller pressor effect and a lesser constrictor action on the renal and mesenteric vascular beds; it did not constrict the hindquarters vascular bed. 8. These results show, that in conscious Long Evans and Brattleboro rats, the initial depressor effects of the higher bolus doses of endothelin-1 and -3 were similar, and, hence, not influenced by the absence of endogenous vasopressin. Endothelin-1 and -3 appear equipotent in their initial hyperaemic vasodilator effects in the hindquarters vasculature in both strains, making it unlikely that this effect is dependent on the release of atrial natriuretic peptide (ANP), since ANP does not cause significant increases in hindquarters blood flow in Brattleboro rats. The greater delayed pressor effect of endothelin-1 is associated with its more marked vasoconstrictor effects on renal and mesenteric vascular beds and is accentuated, relative to endothelin-3, by the lack of a constrictor effect of endothelin-3 in the hindquarters vasculature.
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PMID:Regional haemodynamic effects of endothelin-1 and endothelin-3 in conscious Long Evans and Brattleboro rats. 213 84


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