Don't underestimate Koch's bacillus.
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Biomedical subjects
Publications and source records attributed to T Morgan.
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1. Physiological concentrations of antidiuretic hormone increase diffusional water permeability but not measurable cyclic AMP content in the isolated papilla of the rat's kidney. 2. Theophylline (6 mM) increases diffusional water permeability and cyclic AMP content in the isolated papilla of the rat's kidney. 3. The increase in water permeability is detected with 5 muunits.ml-1 of ADH and is maximal with 50 muunits.ml-1. The same maximum was achieved with 6 mM theophylline. 4. Cyclic AMP and dibutyryl cyclic AMP both increase water permeability, but to a lesser extent than theophylline or ADH. 5. In the presence of theophylline, ADH causes a dose related generation of tissue cyclic AMP up to a dose of 2,000,000 muunits.ml-1. 6. Adenyl cyclase is increasingly activated by ADH up to doses of 2,000,000 muunits.ml-1. 7. These results suggest that while ADH activates the adenyl cyclase system and changes water permeability there are sufficient disparities to cast doubt on an exclusive role for cyclic AMP as the second messenger.
1. The diffusional permeabilities of collecting duct membranes to THO, 14C-urea and 22Na+ have been measured at different concentrations of urea, NaCl and mannitol. 2. In the absence of urea in perfusate and bath or in its presence in low concentrations, the diffusional permeability to urea was 2.0 (s.e.m. = 0.15, n = 58) micrometer s-1, compared with 0.87 (s.e.m. = 0.06, n = 29) microgram s-1 when 200 mmol/l urea was present. The permeability of the collecting ducts to THO or Na+ was not affected by the different urea concentrations. 3. High concentrations of sodium chloride increased the diffusional permeability of collecting ducts to water and urea but did not affect the diffusional permeability of the collecting duct to Na+. 4. Mannitol had effects similar to those of sodium chloride. 5. In all media tested there was an increase in THO and urea permeability when supramaximal amounts of antidiuretic hormone were added. The increases in the various media for each substance were similar, despite widely different starting permeabilities. 6. The results suggest that solutes and water move across collecting duct epithelium by several pathways that respond differently to various stimuli.
1. Sodium intake was varied in 182 normotensive volunteers. 2. systolic blood pressure rose by 3.3 (s.e.m. = 0.9) mmHg supine, 2.8 (s.e.m. = 0.7) mmHg erect. 3. Diastolic blood pressure rose by 2.7 (s.e.m. = 0.8) mmHg supine, 2.6 (s.e.m. = 0.8) mmHg erect. 4. In people over 50 y the rise was 12.4/8.1 mmHg (supine) and 9.1/7.1 mmHg (erect). 5. Blood pressure rose as sodium intake increased. Most of the rise was in the older patients but about 25% of younger patients were sensitive to sodium.
1. The diffusional permeability of collecting ducts to 22Na+ and 36Cl- was measured in rat papillae in vitro. 2. The permeability of the collecting duct to 36Cl- was 0.72 (s.e.m. = 0.01; n = 356) microns/sec which was significantly higher than the value of 0.51 (s.e.m. = 0.01; n = 356) microns/sec measured for 22Na+. 3. Collecting ducts in papillae taken from rats on a high sodium intake had a 22Na+ permeability of 0.63 (s.e.m. = 0.04; n = 53) microns/sec which was significantly higher than the value on a normal salt intake (0.50, s.e.m. = 0.04; n = 46 microns/sec). 4. When papillae from normal rats were studied in plasma taken from salt loaded rats, the 22Na+ permeability of 0.59 (s.e.m. = 0.04; n = 18) microns/sec was significantly higher than when incubated in plasma from normal rats (0.44, s.e.m. = 0.05; n = 12) microns/sec. 5. An extract of urine with natriuretic activity had no effect on 22Na+ permeability when tested in this system. 6. Adrenalectomy, PGE2, indomethacin and antidiuretic hormone had no significant effect on 22Na+ and 36Cl- permeability. 7. A substance exists in plasma from salt loaded animals that increases the permeability of collecting ducts to sodium. This effect could explain the component of the natriuresis that follows saline infusion which is independent of changes in glomerular filtration rate, aldosterone, or proximal tubule reabsorption.
The collecting ducts in papillae taken from normal rats have a measurable increase in diffusional tritiated water (THO) permeability with ADH 5 mu unit/ml and this increase is maximal with antidiuretic hormone (ADH) 100 mu unit/ml added to media. The presence of plasma from rats pretreated with lithium to make them polyuric inhibited the response to ADH. The lowest concentration of ADH that caused a measurable increase in diffusional water permeability was 50 mu unit/ml and the increase was maximal with ADH 2000 mu unit/ml. The maximum response to ADH did not differ whether plasma from control or lithium pretreated rats was used. However, the dose-response curve to ADH was shifted to the right by the plasma from lithium-pretreated rats. Lithium added to the plasma from control rats did not alter the response to ADH. It is proposed that lithium given to rats causes a circulatory factor to be produced that inhibits in a competitive fashion the response of the collecting duct to ADH. Such an effect would explain many features of the impairment of water excretion associated with lithium use.
Ketanserin, a 5HT2-receptor blocking drug was given to 17 patients with essential hypertension. Satisfactory control was achieved in 13 patients. Control was not as satisfactory when given once daily. There was no rebound effect when the drug was ceased. Side-effects were few. Ketanserin was a satisfactory drug to reduce blood pressure in patients with moderate hypertension.
1. While it is believed that the mammalian distal nephron is not involved in uric acid transport, this has not been directly evaluated. Nevertheless, some studies are consistent with significant distal nephron transport. 2. As uric acid transport in man may be similar to the rat, undirectional uric acid permeability was evaluated by perfusion of the isolated rat papillary collecting duct. 3. Uric acid permeability was 0.61 +/- 0.04 micron/s, which was similar to sodium permeability (0.66 +/- 0.05 micron/s) but was less than chloride permeability (0.93 +/- 0.07 micron/s) and markedly less than water permeability (4.81 +/- 0.21 micron/s). Uric acid permeability was not changed following the addition of a maximal antidiuretic concentration of arginine vasopressin (200 microU/mL), nor was it changed by altering the uric acid concentration in the perfusate and bath. 4. These results demonstrate that the papillary collecting duct is permeable to uric acid. The coefficient of transport is sufficiently low and insensitive to arginine vasopressin and uric acid concentrations to suggest that any transport that occurs is probably passive and only of minor physiological significance.
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Cardiac hypertrophy is an independent predictor of morbidity and mortality. The exact relationship between blood pressure, hormones and cardiac hypertrophy is unclear. This study was undertaken to determine if intermittent elevation of blood pressure could cause left ventricular hypertrophy. Blood pressure was elevated intermittently by intraperitoneal injections of angiotensin II, noradrenalin and methoxamine. Blood pressure was acutely elevated by 60 mmHg or more for periods lasting up to 1 hour on up to 4 occasions each day. Cardiac index was measured 2 and 4 weeks after the experiment started. The cardiac index was increased by all procedures. The results were complicated by a retardation of growth in some experimental groups, meaning that the cardiac weight did not increase though the index did. In a study looking at the interaction of sodium and angiotensin II high sodium intake caused left ventricular hypertrophy and injections of angiotensin II caused further left ventricular hypertrophy. This study indicated that acute intermittent elevation of blood pressure could cause left ventricular hypertrophy and suggests that wall stress rather than 24 hour workload is the important triggering mechanism.