Plasma inhibitors of Na,K-ATPase: relation to salt balance and hypertension.
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Animals↗
Biomedical subjects
V M Buckalew
Publications and source records attributed to V M Buckalew.
Hyponatremia: pathogenesis and management.
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Absorption↗
Analgesic nephropathy: a significant cause of morbidity in the United States.
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Analgesics↗
Renal disease from habitual antipyretic analgesic consumption: an assessment of the epidemiologic evidence.
The quantitative evidence relating habitual antipyretic analgesic consumption to the development of renal disease is reviewed. For purposes of analysis, "abuse" of analgesics is defined as regular, usually daily consumption. The prevalence of habitual consumption demonstrates marked geographic variation for poorly defined reasons. Prevalence tended to be highest in those populations in which phenacetin was available and popular. The prevalence of nephropathy among habitual consumers also shows marked interpopulation variability. A highly significant linear relationship exists between the prevalence of habitual analgesic consumption in a given population and the prevalence of nephropathy in the subset of that population that habitually consumes analgesics. This relationship may represent a dose-response curve relating amount of analgesic intake to prevalence of nephropathy. Four cross-sectional studies, 1 longitudinal, and 1 case-control study have shown significant differences in prevalence of nephropathy between habitual users of phenacetin-containing analgesics and control populations. Conversely, 2 cross-sectional studies and 1 case control study showed no difference between habitual users of analgesics and control populations. However, those studies showing no difference were performed in populations with low prevalence of habitual consumption of compound analgesics and a lower prevalence of nephropathy than was found in those populations where differences were observed. The relative risk for developing various manifestations of analgesic nephropathy has been estimated in 4 studies and varies depending on which abnormality is considered. Data are available only for subjects consuming phenacetin-containing compound analgesics. The relative risk for elevated serum creatinine is in the range of 8 to 11, about twice that for an abnormal renal concentrating test (approximately 4). The relative risk for clinical papillary necrosis is approximately 18, and for cause-specific death (and by inference for end-stage renal disease) about 4. The difference in risk between most clinical manifestations of analgesic nephropathy and death (or end-stage renal disease) may be due to the fact that most patients with nephropathy do not progress to terminal renal failure. Rheumatology clinic studies indicate that the prevalence of nephropathy in habitual consumers of phenacetin-containing compounds is higher than that for habitual consumers of aspirin alone. Removal of phenacetin from compound analgesics in Scandinavian countries appears to have reduced the prevalence of papillary necrosis and death from interstitial nephritis.(ABSTRACT TRUNCATED AT 400 WORDS)
Anti-Inflammatory Agents, Non-Steroidal↗
Plasma levels of an ouabain-like factor associated with an increased incidence of cerebral haemorrhage in one-kidney, one wrap hypertension in rabbits.
To examine the role of an ouabain-like factor (OLF) in the pathogenesis of cardiovascular disease in hypertension, we examined plasma levels of OLF in a malignant form of one-kidney, one wrap (1K,1W) hypertension. Two weeks after the induction of hypertension plasma OLF increased to 282% compared to control animals. Additionally, blood pressure, the cardiac index, incidence of cerebral haemorrhage and vascular aneurysms were increased. Blood pressure was found to be inversely correlated with cardiac hypertrophy. No correlations between plasma OLF and blood pressure, cardiac hypertrophy or vascular aneurysms were found. However, hypertensive animals with cerebral haemorrhage had significantly higher plasma OLF than animals without cerebral haemorrhage. These results suggest that high plasma OLF in hypertensive subject may increase the risk of cerebral haemorrhage.
Animals↗
The incidence of diuretic-induced hypokalemia in two distinct clinic settings.
We studied the incidence of diuretic-induced hypokalemia (DIH) in two diuretic-treated hypertensive populations. Thirty-seven patients with mild hypertension were treated with HCTZ and monitored over 6 months. Group 1 (21 patients) was treated with 25 mg HCTZ q.d. in a public hypertension clinic. Group 2 (16 patients) was treated with 50 mg HCTZ q.d. in a private-practice setting. Group 1 was predominantly nonwhite (76% vs. 31% [p less than 0.002]). Baseline serum potassium levels were lower in group 1 (3.93 vs. 4.42 mEq/L [p less than 0.001]). Equivalent reductions in blood pressure and serum potassium were observed in both groups. Contrary to expectations, DIH (serum potassium less than 3.5 mEq/L) developed in 52% of group 1 and 19% of group 2 (p = 0.037). Black females were especially at risk for DIH. The higher incidence of DIH in group 1 appears to be related to lower baseline serum potassium levels.
Adolescent↗
Complete distal renal tubular acidosis in systemic lupus: clinical and laboratory findings.
We report two patients with systemic lupus erythematosus (SLE) who were found to have complete (acidotic) distal renal tubular acidosis (DRTA). One patient had nephrocalcinosis and renal magnesium wasting with tetany; the other patient had nephrolithiasis and nephrotic syndrome secondary to membranous glomerulopathy. Both patients had decreased urinary citrate excretion but neither had hypercalciuria. We discuss the association of DRTA with immunologic disorders and the possible role of hypocitraturia in promoting renal calcification in these patients. We suggest that patients with renal calcification be evaluated for DRTA, and that patients found to have DRTA be further evaluated for signs, symptoms, and laboratory evidence of immunologic disorders.
Acidosis, Renal Tubular↗
Gamma-2MSH is natriuretic in the rat.
Previous reports suggest that peptides containing an amino acid sequence similar to that of ACTH-(4-10) increased Na excretion in the rat. gamma 2MSH contains such a sequence. An in vivo rat bioassay for natriuretic factors was employed to demonstrate the natriuretic action of gamma 2MSH. A significant natriuretic effect was observed, with a peak response 30-50 min following the bolus injections of 0.64, 6.4 or 64 pmol, but not with smaller or larger amounts of gamma 2MSH. A kaliuretic and diuretic action of gamma 2MSH was not consistently evident. gamma MSH may represent an endogenous compound involved in the physiological regulation of Na excretion.
Animals↗
A digoxin-like immunoreactive substance in preeclampsia.
A study has been undertaken of levels of an endogenous substance which immunologically cross reacts with digoxin and may be the putative natriuretic hormone. The possibility that this substance may play a role in the pathophysiology of preeclampsia has been studied by measuring the plasma concentrations in clinically healthy and preeclamptic pregnant patients. A significant difference (p less than 0.001) between these two groups has been found.
Cross Reactions↗
Endocrinologic effects of antihypertensive therapy with guanabenz or hydrochlorothiazide.
The effect of antihypertensive therapy with guanabenz or hydrochlorothiazide (HCTZ) on the secretion of growth hormone, prolactin, insulin, and glucagon was evaluated in double-blind fashion in 45 patients. Fifteen patients were treated with HCTZ, 50 mg twice daily, and 30 patients were treated with twice-daily dosages of guanabenz ranging from 4 to 32 mg. Blood samples for hormone analysis were collected during maintenance therapy when blood pressure was controlled as well as 1 week after the withdrawal of the antihypertensive medications. Serum levels of growth hormone and prolactin were within the normal ranges and were unchanged during treatment with HCTZ or guanabenz at any dose level. Interpatient variability in insulin levels was high, although within-subject insulin levels generally were consistent. No treatment effects were seen for insulin levels among guanabenz- or HCTZ-treated patients. Glucagon levels generally were above the expected range for fasting patients and were lower in patients receiving 4 or 8 mg of guanabenz twice daily than in those receiving 16 mg twice daily (p less than 0.05) and in those treated with HCTZ (p less than 0.01). However, analysis of paired data revealed no changes in glucagon levels upon withdrawal of guanabenz, whereas glucagon levels were higher during HCTZ treatment than after drug withdrawal (p = 0.012). Since guanabenz treatment did not affect the secretion of pancreatic or pituitary hormones, it may be preferable to other centrally acting agents and thiazide diuretics for hypertensive patients who are elderly, overweight, or diabetic.
Adult↗
Effect of guanabenz withdrawal on blood pressure and plasma catecholamines.
Previous studies provide conflicting conclusions concerning the consequences of abrupt withdrawal of guanabenz therapy for essential hypertension. In the present study, 10 patients were treated for mild to moderate essential hypertension for 12 weeks, following which the drug was abruptly withdrawn. Blood pressure, pulse rate, and plasma catecholamine levels were obtained before, at 4 and 12 weeks after starting therapy, and 48-96 h and 4 and 8 weeks post-therapy. At the end of 12 weeks of therapy, the mean dose of guanabenz was 22.2 +/- 4.4 mg/day (range, 16-48 mg/day) and supine blood pressure was 140 +/- 5.5/88 +/- 2.4 mm Hg. Two to 4 days after drug withdrawal, supine and standing diastolic blood pressure remained significantly reduced compared to control (p less than 0.01). Standing systolic blood pressure also remained significantly reduced compared to control (p less than 0.01). Mean plasma catecholamine level was less than baseline after 4 weeks of therapy, but the change was not significant. No increase in plasma catecholamine concentration was observed at any time during the withdrawal period. No patient had symptoms of sweating, nervousness, palpitations, or insomnia after guanabenz withdrawal. In one patient with pretreatment systolic pressure of 150 mm Hg, systolic pressure 48 h after drug withdrawal was 160 mm Hg. These studies, together with previous reports, suggest that guanabenz therapy for mild to moderate essential hypertension in doses of 32 mg/day or less can be safely withdrawn on an outpatient basis with a very low incidence of withdrawal phenomena.
Blood Pressure↗
Ion transport characteristics in rhesus monkey erythrocytes: relationship to age and blood pressure.
Erythrocyte (RBC) ion transport characteristics were examined in six young Rhesus monkeys (RM) age 3.3 +/- .3 (means +/- S.D.) years and seven mature RM 15.4 +/- 1 (means +/- S.D.) years. It was found that the older RM when compared to the younger RM demonstrated significantly elevated mean arterial pressures (MAP) (96 +/- 15 versus 75 +/- 11 mmHg), RBC intracellular sodiums (RBC Nai) (16.2 +/- 4 versus 11 +/- 3 mEq/liter RBC) and NaK ATPase pump rates per RBC (PR) (PR = ouabain sensitive K uptake divided by ouabain binding sites per RBC) (104 +/- 18 versus 83 +/- 18 K+ ions/sec/pump unit). However, it was also found that when the data from both groups were pooled and collectively analyzed a significantly positive correlation could be found between MAP and RBC Nai (p less than .001, r = .82), MAP and PR (p less than .01, r = .67) as well as PR and RBC Nai (p less than .001, r = .76). The fact that positive correlations exist among these parameters, independent of age, would suggest that while MAP, RBC Nai and PR tend to be elevated with advancing age, these abberations are not invariable consequences of age and best reflect the pivotal abberration of rising Nai. While insufficient data exist to account for the rise in Nai and no cause-effect relationship can be established it is clear that rising MAP and PR correlate best with rising Nai.
Age Factors↗
Sodium, water, and congestive heart failure.
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Captopril↗
Renal alpha 1- and alpha 2-adrenoceptor mediated vasoconstriction in dogs: comparison of phenylephrine, clonidine, and guanabenz.
The alpha 2-agonist, guanabenz, increases Na and water excretion with little change in renal blood flow, while clonidine has been reported to cause antinatriuresis proportional to renal vasoconstriction. We hypothesized that clonidine-mediated renal vasoconstriction involves alpha 1-receptors. Dose-response curves were constructed correlating decreases in renal blood flow with doses of phenylephrine, clonidine, and guanabenz injected as boluses into renal arteries of anesthetized dogs. Changes in renal blood flow before and after prazosin, yohimbine or verapamil were recorded. Guanabenz was a 10-fold weaker vasoconstrictor than clonidine, but was still effective when alpha 1-receptors were blocked. Tenfold differences were found between phenylephrine, clonidine, and guanabenz for dependence on alpha 1-receptors. Denervation did not significantly shift the curves. Verapamil markedly attenuated only clonidine and guanabenz, which supported their dependence on calcium channels for vascular smooth muscle contraction. Thus, postsynaptic alpha 2-adrenoceptors can contribute to renal vasoconstriction in the dog but the receptors are either less numerous on the vasculature or are less efficiently coupled to contractile elements than are alpha 1-receptors. Clonidine constricts the renal vasculature through both adrenoceptor subtypes.
Animals↗
Renal alpha 1- and alpha 2-adrenoceptor mediated vasoconstriction in dogs.
Clonidine (C) and guanabenz (G) are both alpha 2-agonists. Whereas C has been reported to cause anti-natriuresis proportional to renal vasoconstriction with acute infusion, G increases sodium and water excretion with little change in renal blood flow (RBF). C-mediated vasoconstriction may involve alpha 1-receptors. RBF in anaesthetized dogs was measured electromagnetically. Boluses of phenylephrine (P), C and G were injected into the renal artery via a perfusion cannula. Responses were expressed as delta RBF. Then prazosin or yohimbine were administered intra-arterially and dose-response curves repeated. The shift in dose ratio (delta ED50 after prazosin/yohimbine) for P was 52.9, for C was 4.7 and for G was 0.62. G was a 10-fold weaker vasoconstrictor than C, but G was still effective when alpha 1-receptors were blocked. Ten-fold differences were found between P, C and G for dependence upon alpha 1-adrenoceptors. Denervation did not significantly shift the curves. Thus, postsynaptic alpha 2-receptors can contribute to renal vasoconstriction, but the receptors are either less numerous or less efficiently coupled to contractile elements than in other beds. Verapamil markedly attenuated responses to C and G. Since tubular alpha 1-receptors have also been implicated in sodium transport, C may be more prone than G to cause anti-natriuresis both through stimulated tubular reabsorption and renal vasoconstriction.
Animals↗
Studies of a digitalis-like autacoid in dog plasma.
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Animals↗
Preoptic-hypothalamic periventricular lesions reduce natriuresis to volume expansion.
The present experiment was designed to determine if electrolytic ablation of the periventricular tissue surrounding the anteroventral third ventricle (AV3V) altered the natriuresis typically seen during isotonic volume expansion. Control and AV3V-lesioned rats received intravenous infusions of 0.9% NaCl at 0.5 ml/min until 10% body weight was given. Arterial blood pressure was monitored, and urine was collected throughout the experiment. Following expansion, blood was processed for analysis of natriuretic hormonelike activity by chromatographic separation of plasma extracts followed by measuring antinatriferic activity across the isolated toad bladder. Urinary sodium excretion and urine volume during expansion were significantly less in rats with lesions surrounding the AV3V region than in control rats. Toad bladder bioassay showed a high level of natriuretic hormonelike activity in control animals following volume expansion, but no natriuretic hormonelike activity in plasma from volume-expanded rats with AV3V lesions. These data demonstrate that AV3V periventricular ablation attenuates the natriuresis induced by isotonic-volume expansion. In addition, preliminary results indicate the AV3V region may be a central site critical for natriuretic hormonelike activity and control of extracellular fluid volume.
Animals↗