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Biomedical subjects

C R Lake

Publications and source records attributed to C R Lake.

At least 127 records · Page 7Linked to original sources
PubMed1980

Effects of moderate short-term potassium depletion in normal humans. The role of prostaglandins.

The role of prostaglandins (PG) in the effects of potassium (K+)depletion was studied in six normal women. A mean K+-deficit of 220 mEq was induced with and without concomitant treatment with indomethacin (150 mg/day). Mean serum K+ concentration decreased from 4.2 +/- (S.E.) 0.1 to 3.2 +/- 0.1 mEq/L without indomethacin and from 4.1 +/- 0.1 to 3.2 +/- 0.1 mEq/L with indomethacin. "Supine" and "upright" plasma renin activity (PRA) and plasma norepinephrine concentration (NE) were unaltered by K+ -depletion alone but decreased with indomethacin. Plasma aldosterone (PA) was suppressed during K+-depletion (control: 7.2 +/- 2.6 ng/dl supine, 19.3 +/- 8.1 ng/dl upright; K+-depletion: 2.6 +/- 0.3 ng/dl supine, 5.5 +/- 1.3 ng/dl upright) and was paralleled by a decrease in urinary aldosterone. K+- depletion decreased urinary PGE2 from 667 +/- 133 to 343 +/- 60 ng/day (P less than 0.025) without a change in PGF2 alpha. The dose of exogenous angiotensin II (A II) which increased diastolic blood pressure by 20 mm Hg (pressor dose) was 7.1 +/- 1.4 ng/kg/min during control and increased to 11.0 +/- 0.7 ng/kg/min during K+-depletion (P less than 0.05). Indomethacin increased the sensitivity to A II both during control (pressor dose: 4.9 +/- 0.6 ng/kg/min) and K+ - depletion (pressor dose: 6.0 +/- 1.0 ng/kg/min). These results indicate that in healthy subjects, moderate short-term K+-depletion does not affect PRA or NE but decreases production of aldosterone and PGE2 by the kidney. The changes in vascular sensitivity to exogenous A II during K+-depletion and indomethacin and the decreases in plasma NE and PRA during indomethacin may be explained by changes in vascular vasodilator PG.

Aldosterone↗
PubMed1980

Fenfluramine potentiation of antihypertensive effects of thiazides.

Hydrochlorothiazide, a drug which is often initially prescribed for mild to moderate hypertension, failed to lower blood pressures in 9 of 43 patients but concomitantly elevated plasma norepinephrine (NE) levels in all patients with hypertension. The 9 obese hydrochlorothiazide-resistant patients were then given fenfluramine, an anorectic, in addition to the thiazide. They were reevaluated after 2 and 5 wk, at which times there were reductions in blood pressures and marked reductions in the plasma NE levels which had been elevated by the hydrochlorothiazide. Since iatrogenic sympathetic activation seems undesirable in treating hypertension, fenfluramine may be useful in obese thiazide-resistant hypertensive patients when used in combination with a thiazide diuretic.

Antihypertensive Agents↗
PubMed1980

Dissociation between central and peripheral noradrenergic activity in essential hypertension.

1. Eleven patients with essential hypertension and nine healthy normotensive volunteer subjects, all without a neurological disorder, had blood drawn and cerebrospinal fluid sampled for analysis of noradrenaline (NA). 2. Cerebrospinal fluid NA levels were elevated (P < 0.01) in the hypertensive patients but plasma levels of NA were similar between groups. 3. The results suggest there is noradrenergic hyperactivity in the central nervous system which is not reflected in abnormal peripheral sympathetic nervous system function in this group of patients.

Adult↗
PubMed1980

Norepinephrine and gamma-aminobutyric acid in amyotrophic lateral sclerosis.

Patients with amyotrophic lateral sclerosis have increased levels of the neutrotransmitter norepinephrine in blood and cerebrospinal fluid and depressed levels of the inhibitory neurotransmitter gamma-aminobutyric acid in cerebrospinal fluid. These neurochemical alterations are most marked in patients bedridden with advanced disease, appear interrelated, and lead to cardiovascular alterations in patients with amyotrophic lateral sclerosis.

Adult↗
PubMed1979

Norepinephrine elevations in cerebrospinal fluid after d- and l-amphetamine.

We continuously collected cerebrospinal fluid (CSF) from the lateral ventricles of monkeys and gave them from 0.1 to 1.0 mg/kg d- or l-amphetamine intravenously. The norepinephrine (NE) content of their CSF had a small circadian rhythm and a large increase after amphetamine. 1.0 mg/kg amphetamine gave a four-fold rise in CSF-NE which remained elevated for 33 h, smaller doses gave proportionately lesser responses. Both d- and l-amphetamine caused similar NE elevations except for minor differences at the highest dose. If there are differences in behavioral effects of moderate doses of d- and l-amphetamine, they are probably not due to a general difference in central NE release from these stereoisomers.

Amphetamine↗
PubMed1979

Hyperthermia potentiates doxorubicin-related cardiotoxic effects.

The intercurrent administration of doxorubicin hydrochloride to a patient undergoing whole-body hyperthermia for the treatment of metastatic cancer repeatedly produced ventricular irritability and cardiac dysfunction. Individually, doxorubicin and hyperthermia were tolerated by the patient without incident. Catecholamine determinations showed that the administration of doxorubicin under hyperthermic conditions increased the liberation of both epinephrine and norepinephrine. The acute synergistic cardiotoxic effects occurred with doxorubicin dosages that were severalfold less than those associated with only mild and transient ECG disturbances under normothermic conditions.

Arrhythmias, Cardiac↗
PubMed1979

Electrolytes and norepinephrine levels in blood of patients with cystic fibrosis.

Young adults with cystic fibrosis in good to excellent condition have reduced plasma sodium and chloride and elevated plasma potassium compared to a group of healthy young adult control subjects. Blood pressure was also lower in the patients with cystic fibrosis. However, plasma norepinephrine and dopamine-beta-hydroxylase and their response to standing and isometric hand grip were normal in the cystic fibrosis patients.

Adolescent↗
PubMed1979

Bromocriptine inhibits norepinephrine release.

Bromocriptine is a dopamine agonist that induces postural hypotension and can be used as an antihypertensive. The drug inhibits release of norepinephrine (NE) from an isolated artery by stimulating presynaptic receptors. In normotensive subjects it lowers both plasma and cerebrospinal fluid (CSF) levels of NE by 50% and lowers blood pressure moderately in standing subjects and slightly in recumbent subjects. Through central and peripheral mechanisms, bromocriptine inhibits sympathetic nervous discharge of NE.

Adult↗
PubMed1979

Hydrochlorothiazide-induced sympathetic hyperactivity in hypertensive patients.

Hydrochlorothiazide-induced diuresis and natriuresis is considered to be responsible for the antihypertensive effect of this drug. After short-term treatment there is decreased cardiac output and increased peripheral resistance which we have found to be attended by increased plasma norepinephrine (NE) levels. After longer treatment cardiac output returns to normal and peripheral resistance declines. At this time, plasma NE levels remain elevated, indicating that peripheral resistance reduction is not a consequence of a reduction of the elevated level of sympathetic activity. These results provide a rationale for the combined use of diuretics and drugs which diminish noradrenergic activity in the treatment of hypertension.

Adult↗
PubMed1979

Effect of imipramine on norepinephrine and blood pressure in enuretic boys.

The effect of imipramine, desmethylimipramine, and methscopolamine on blood pressure (BP) and plasma norepinephrine (NE) was measured in enuretic boys in a double-blind, placebo-controlled study. Measurements were obtained on the thirteenth day of medication (75 mg at bedtime). The tricyclic drugs induced a rise in diastolic BP as well as an increase in plasma NE but there was no significant relationshhip between the increments in plasma NE and BP. The plasma concentration of drug correlated with the drug-induced BP rise. This is the fifth study to demonstrate a hypertensive effect of tricyclic drugs in children in contrast to the systolic hypotension usually seen in adult patients. It is not clear from our data whether children have different cardiovascular compensatory reflexes or whether they experience a greater stimulant effect from the drug.

Blood Pressure↗