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Biomedical subjects

T O Morgan

Publications and source records attributed to T O Morgan.

At least 73 records · Page 4Linked to original sources
PubMed1989

Magnesium supplementation in mild hypertensive patients on a moderately low sodium diet.

1. The effect of oral magnesium supplementation was assessed in a group of untreated, mild hypertensive subjects who were following a moderately low sodium diet (baseline urinary sodium 86 +/- 6 mmol/day). 2. Thirteen patients were allocated placebo and 12 were allocated magnesium aspartate (10 mmol/day) in a double blind fashion for 8 weeks. 3. There was no fall in blood pressure with magnesium supplementation and no significant difference in blood pressure between groups at the end of the study. 4. In the magnesium group there was an increase in urinary magnesium (4.4 +/- 0.6 to 6.1 +/- 1 mmol/day P less than 0.001), and urinary calcium (4.3 +/- 0.7 to 5.5 +/- 0.9 mmol/day P less than 0.01). There was no change in plasma or red cell magnesium or plasma renin activity with supplementation. 5. Magnesium supplementation does not appear to have an additive hypotensive effect in mild hypertensive subjects on a reduced sodium intake.

Aged↗
PubMed1989

Effect of converting enzyme inhibition on renin synthesis and secretion in mice.

We have investigated the relative importance of renal renin stores and de novo synthesis during stimulation of renin secretion and the role of transcription and posttranscriptional factors in providing increased synthesis of renin. When enalapril was administered to previously untreated mice, plasma renin concentration increased 40-fold within 1.5 hours, and remained at a high level for the 8 days of the experiment. Renal renin decreased by 82% after 24 hours and thereafter increased to levels higher than controls. Calculations of renin turnover, based on data for the rate of metabolism of renin in plasma, indicated that most of the renin released in the first 24 hours could be accounted for by the decrease in renal renin stores, indicating that de novo synthesis played only a minor role. After 24 hours, however, when both plasma renin concentration and renal renin increased, the calculated rate of renin synthesis increased to nearly 40 times the rate in controls. When enalapril was administered to mice that had been depleted of plasma and renal renin by chronic sodium loading, plasma renin concentration increased markedly within 1.5 hours, but to only half the level achieved in the previously untreated mice. No decrease in renal renin occurred, suggesting that the renal renin remaining after chronic sodium loading was not available for release. Renal renin messenger RNA increased 4.5-fold after 6 hours, and after 8 days had increased to 5.0 times the level at day 0. The increase in calculated rate of renin synthesis was maximal between 5 and 8 days, when it was 54 times greater than at day 0. During enalapril treatment, there were marked increases in the granulation of the juxtaglomerular cells and in the amount of rough endoplasmic reticulum and Golgi apparatus they contained. These results suggest that posttranscriptional factors play a major role in determining the rate of renin synthesis.

Analysis of Variance↗
PubMed1988

Influence of angiotensin II (AII) and angiotensin I (AI) on renal renin synthesis and release.

This study examined the effect of exogenous AI and AII on renin synthesis and release. AII or AII + AI were given using osmotic minipumps, over a 7 day period to rats receiving oral Enalapril. Enalapril caused a marked increase in renin release and synthesis. AII abolished the rise in plasma and renal renin observed with Enalapril. AI had no inhibitory or stimulatory effect on renin release or synthesis in rats receiving Enalapril and AII.

Angiotensin I↗
PubMed1988

Age-related changes in angiotensin II-stimulated proximal tubule fluid reabsorption in the spontaneously hypertensive rat.

The development of hypertension in the spontaneously hypertensive rat (SHR) up to 8 weeks of age involves sodium retention with reduced fractional sodium excretion. Since angiotensin II (Ang II) directly stimulates proximal tubular sodium transport, we investigated age-related changes in proximal reabsorption (Jv), using shrinking split-drop micropuncture before and after enalaprilat in SHR at 5, 7 and 12 weeks of age and in age-matched Wistar-Kyoto rats (WKY). Control values for Jv were higher in the SHR than in WKY at 5 weeks, but lower at 7 and 12 weeks, consistent with an early phase of sodium retention. Enalaprilat reduced mean Jv by approximately 15% in all WKY groups, indicating the extent of Ang II-stimulated transport. In the SHR there was an age-dependent reduction in the effect of enalaprilat on Jv, and by 12 weeks no Ang II stimulation could be detected. Age-related changes in proximal tubular reabsorption could contribute to sodium retention in the young SHR and may reflect a more general pattern of inherited transport defects.

Aging↗
PubMed1988

Angiotensins II and III prevent captopril-induced renin release in the rat.

1. The effects of exogenous angiotensins II and III (50 pmol/min i.v.) on plasma renin release following captopril injection (5 mg/kg, i.v.) were studied in anaesthetized Sprague-Dawley rats, to determine whether angiotensin II blockade is the major mechanism by which captopril induces renin release. 2. Captopril produced a 12-fold increase in plasma renin concentration compared with saline-injected controls. This was completely reversed by pre-infusion of angiotensin II or III. 3. The fall in blood pressure following captopril treatment was also abolished by angiotensins II and III pre-infusion. Noradrenaline pre-infusion (200-800 ng/min, i.v.) also prevented the captopril-induced hypotension but did not alter the rise in plasma renin. 4. Ureteric ligation did not significantly reduce captopril-induced renin release suggesting that acute changes in sodium excretion or delivery of electrolyte to the macula densa were not involved in renin release. 5. These findings suggest that captopril induces renin release by inhibiting angiotensin II feedback control of renin secretion and that angiotensin III may also modulate renin release.

Angiotensin II↗
PubMed1988

Change in blood pressure in relation to change in nutrients effected by manipulation of dietary sodium and potassium.

1. As part of a study investigating the effect of dietary alterations of sodium and potassium intake on blood pressure, the changes in nutrients that occurred with dietary intervention were determined. 2. Mild hypertensive subjects were randomized to one of four dietary intervention groups: control; high potassium; low sodium; low sodium, high potassium. The changes in nutrients in each diet group were assessed by dietary history and five repeat 24 h dietary recalls. Assessment was validated by measurement of urinary nitrogen excretion and urinary electrolytes. 3. The three dietary intervention groups experienced a fall in blood pressure (systolic: 4.4 +/- 1.0 mmHg, P less than 0.005; diastolic: 3.3 +/- 0.7 mmHg, P less than 0.001), greater than that observed in the control group. 4. The only significant dietary change across all diet groups was a reduction in the dietary sodium/potassium ratio, which was significantly less than that of the control group. The only other nutrient to differ from the control in all groups was fat intake, which was reduced. 5. In the control group there was a small but significant decrease in energy, fibre, protein, carbohydrate, potassium and magnesium intake. In the high potassium group there was a significant increase in fibre, carbohydrate, potassium, magnesium, and a decrease in calcium intake. In the low sodium group there was a decrease in energy intake with a subsequent reduction in all nutrients except alcohol. In the low sodium, high potassium group there was a significant reduction in dietary sodium and protein and an increase in fibre, carbohydrate, potassium and magnesium. 6. The reduction of the dietary sodium/potassium ratio correlated with a reduction in the urinary sodium/potassium ratio. This was the best predictor for change in diastolic pressure in all groups, suggesting that reduction in the sodium/potassium ratio contributed to the fall in blood pressure. 7. Reduction of sodium intake and increase in potassium intake by dietary means caused a reduction in blood pressure which does not appear to be due to alteration of other measured dietary constituents.

Alcohol Drinking↗
PubMed1988

High salt diet decreases longevity in the spontaneously hypertensive rat.

1. Blood pressure, body weight and mortality rate were examined in female spontaneously hypertensive rats (SHR) of the Okamoto strain maintained on a lifelong high (5% NaCl w/w) or low (0.1% NaCl w/w) salt diet. 2. A high salt diet increased mortality and decreased body weight in SHR, but failed to significantly alter blood pressure up to 24 months of age. 3. Hence, a low salt diet does not appear to be a long-term risk factor and may protect the SHR from cardiovascular accidents.

Animals↗
PubMed1988

Injury severity scoring: influence of timing and nurse raters on accuracy.

The Abbreviated Injury Scale (AIS) and its incorporation into the Injury Severity Score (ISS) have become accepted as objective ways to quantitate the severity of trauma. To examine the practicality of using critical care nurses to initiate injury scoring within the first 24 hours of admission, a prospective study was undertaken. Nurses on the trauma intensive care unit were asked to calculate the ISS in patients admitted to the unit over a 4-month period. Scoring was completed within 24 hours of admission and recorded on an edited single-page chart constructed from the 1980 revision of the AIS. All patients were followed up until discharge, and the ISS was reviewed in the light of discharge diagnoses. One hundred four patients were studied, and accurate scores were calculated in 54 patients (51.9%). In three patients (2.9%) the single-page chart did not allow accurate scoring, and in 18 patients (17.3%) the diagnoses noted subsequent to the scoring time frame resulted in inaccuracy. Human errors resulted in inaccuracy in 28% of patients. In comparison with a concurrent study involving surgical residents, human error rates were similar. However, scoring within 24 hours, as opposed to 72 hours, resulted in significantly more errors related to diagnostic uncertainty. Initiation of the scoring process soon after admission, with subsequent correction during the hospital course, allows important information to be available at the earliest time.

Clinical Competence↗
PubMed1987

Use of sodium restriction and enalapril in persons with moderate to severe hypertension.

One hundred and seventy-four patients who were receiving drug therapy for hypertension were asked to restrict their sodium intake for three months. At the end of that time their drug therapy was replaced with enalapril and the dose of the drug "titrated" to obtain a diastolic blood pressure of less than 90 mmHg. Sodium restriction caused a small fall in blood pressure and could be used as sole therapy in only 6% of patients. Enalapril therapy was instituted without problems and control of blood pressure below 90 mmHg was achieved in 62% of persons with monotherapy. The number of tablets of enalapril that were taken was reduced from 5.9 to 2.7; in most patients these were taken once a day. There were few side-effects and no depression of white cell count, no proteinuria and no deterioration of renal function. Seventy-six per cent of patients preferred the new regimen either because they felt better than with their previous therapy (52%) or because of the more simple regimen (24%). Enalapril was an effective, well tolerated antihypertensive agent and potentially has a major role to play in the management of patients with high blood pressure.

Antihypertensive Agents↗
PubMed1987

Digital image capture and analysis for split-drop micropuncture.

A method for automated image capture and analysis of shrinking drop sequences is described. The procedure can be managed by a single operator and allows estimates of proximal tubule volume flux to be calculated during the experiment. Speed of analysis is increased considerably (mean time 1.5 min per sequence) compared with previous methods. The potential exists for measurement of droplets in tubules that follow a tortuous path in the horizontal plane and further increases in capture and analysis rate would allow estimation of volume flux under non-steady state conditions. Film processing is eliminated and the removal of operator errors, bias and fatigue associated with manual measurement, coupled with the greatly reduced time required for analysis of sequences makes the shrinking drop method much more reliable and attractive.

Animals↗
PubMed1987

Prenatal high salt diet increases blood pressure and salt retention in the spontaneously hypertensive rat.

1. An examination was made of the effect of prenatal, high salt (5% w/w) and low salt (0.1% w/w) diet on the blood pressure and ability to excrete a salt load of mature spontaneously hypertensive rats (SHR) of the Okamoto strain maintained on normal salt (0.8% w/w) diet after weaning. 2. Prenatal high salt diet resulted in a significant exacerbation of the hypertension of 4 month old SHR when compared with animals given prenatal low salt diet. 3. Three month old SHR given prenatal, high salt diet exhibited a significantly reduced Na+ excretion following a single, oral salt load (150 mmol/l, 1% bodyweight) when compared with the low salt group. 4. Thus, prenatal, high salt diet may influence body fluid homeostasis in genetically susceptible individuals later in life.

Animals↗
PubMed1987

Felodipine versus prazosin as an addition to a beta-blocker in the treatment of essential hypertension. The Australian Multicentre Study.

The efficacy and tolerability of felodipine and prazosin were compared in a double-blind randomised parallel group study of 100 patients with moderately severe essential hypertension, treated concomitantly with a beta-blocking drug. After a 2- to 8-week run in phase (beta-blocking drug plus placebo), patients with a diastolic blood pressure greater than or equal to 95mm Hg were randomly given felodipine (n = 50) or prazosin (n = 50). After an initial dose of either felodipine 2.5mg bid or prazosin 0.5mg bid for 3 days, the drugs were titrated at 2-week intervals (felodipine 5, 10, 20mg bid, prazosin 1, 2, 4mg bid) if the supine diastolic blood pressure was greater than or equal to 90mm Hg. Treatment was continued for 8 weeks. Baseline supine blood pressures of each group were similar (177/104mm Hg, felodipine; 176/103mm Hg, prazosin). At week 6, supine blood pressures in the felodipine group were 144/82mm Hg and 161/90 in the prazosin group. The reductions in systolic and diastolic blood pressures were significantly greater for the felodipine group than the prazosin group in both the supine and standing positions at all visits after baseline. At 8 weeks, supine diastolic blood pressure less than 90mm Hg was achieved in more patients in the felodipine (36/47) than in the prazosin group (20/43, p less than 0.01). The total number of adverse reactions was similar in both groups. During active therapy, a greater number of patients experienced vascular adverse reactions (oedema and flushing) with felodipine (23) than with prazosin (12). Most events were mild and did not necessitate withdrawal from therapy. There were no clinically significant changes in laboratory variables in either treatment group. Felodipine was an effective, well tolerated hypotensive agent when used concomitantly with a beta-blocking drug. In the doses used it was more effective than prazosin at reducing blood pressure.

Adrenergic beta-Antagonists↗
PubMed1987

Captopril attenuates diuretic and natriuretic actions of furosemide but not atrial natriuretic peptide.

Atrial Natriuretic Peptide (ANP) exerts a potent diuretic and natriuretic action in rat, dog and man. To test whether these actions of ANP are due to antagonism of the antinatriuretic actions of endogenous angiotensin II, an examination was made of the renal actions of ANP in anesthetized rats with and without captopril pretreatment. Captopril treatment did not alter the diuretic and natriuretic action of a single, intravenous bolus injection of ANP (1000 ng of the 8-33 ANP). Captopril treatment did significantly attenuate the diuretic and natriuretic actions of Furosemide (20 mg/kg ip). This attenuation was not reversed by concomitant, exogenous angiotensin II infusion. These results suggest that while ANP exerts its renal actions independently of the circulating renin-angiotensin system the diuretic and natriuretic action of Furosemide is modulated by a substrate of angiotensin converting enzyme.

Angiotensin II↗
PubMed1986

Effect of sodium intake and sodium delivery to the macula densa on renal renin content and juxtaglomerular apparatus morphology.

Active and inactive renin were measured in individual juxtaglomerular apparatus (JGA) and in whole kidney homogenates. The morphology of the JGA was examined in microbiopsy glomerular specimens and in kidneys fixed by arterial perfusion. In rats on high and normal salt intake the total renin content of a single JGA was 14 (s.e.m. = 3) and 29 (s.e.m. = 4) ng AI/h, respectively. The amount of cystoplasm occupied by renin granules was 20% and 27%. Crystalline cores were seen in 1.5% and 7% of the granules, respectively. Increased delivery of NaCl to the macula densa did not alter total renin, but decreased inactive renin from 30% to 0, crystalline core-containing cells from 33% to 14% and decreased the percentage of granules with crystalline cores from 12% to 2.2%. Increased sodium in the diet and increased delivery of NaCl to the macula densa decreased the proportion of renin present in the inactive form and decreased the proportion of crystalline cores. These coincidental alterations suggest that crystalline cores contain inactive renin and suggest that the delivery of sodium to the macula densa activates renin.

Animals↗
PubMed1986

Captopril antagonizes the hypotensive action of atrial natriuretic peptide in the anaesthetized rat.

Atrial natriuretic peptide (8-33; ANP) caused a prolonged hypotensive response following intravenous injection in anaesthetized rats. This response was abolished by captopril treatment and restored by concomitant angiotensin II infusion. These results suggest that ANP exerts its hypotensive action in the anaesthetized rat by the antagonism of the vasoconstrictor action of endogenous angiotensin II.

Anesthesia↗