Search PubMed⌕ Search

Biomedical subjects

L Tobian

Publications and source records attributed to L Tobian.

At least 73 records · Page 4Linked to original sources
PubMed1979

A circulating humoral pressor agent in Dahl S rats with salt hypertension.

1. In Dahl S rats becoming hypertensive while on a diet of high NaCl content there appears to be a blood-borne humoral agent which produces vasoconstriction in a bioassay using the isolated hindquarters of rats. 2. This vasoconstrictor effect strongly suggests the presence of a humoral pressor agent or the lack of a vasodilator agent in the blood of hypertensive S rats. 3. The vasoconstrictor effect is not due to high renin concentrations. 4. This humoral vasoconstrictor action could partly account for the high vascular resistance in the hypertensive S rat.

Animals↗
PubMed1979

Evidence for Na-retaining humoral agents and vasoconstrictor humoral agents in hypertension-prone Dahl 'S' rats. Prevention of NaCl-induced hypertension in Dahl 'S' rats with thiazide.

Dahl 'S' rats become hypertensive when fed a high NaCl diet but remain normotensive on a low NaCl diet. Dahl 'R' rats are normotensive on either diet. For a given perfusion pressure, isolated 'S' kidneys excrete 50% less Na than 'R' kidneys. Therefore, we searched for a Na-retaining hormone in 'S' rats. Kidneys were isolated without ischemia from normal rats and were continuously perfused at 125 mm Hg with blood from Dahl 'S' and 'R' rats, all on low NaCl diets. Kidneys and adrenals had been extirpated from the perfusing rats. During 15 min of perfusion, the isolated 'normal' kidneys excreted a mean of 164 micronEq of Na/min/100 g during 26 perfusion experiments with blood from 'R' rats. The 'normal' kidneys excreted a mean of 84 micronEq Na during 24 perfusions with blood from 'S' rats. Thus, the normal kidneys excreted half as much Na when perfused with 'S' blood compared with 'R' blood (p less than 0.02). Seemingly, a Na-retaining humoral agent is present in the blood of 'S' rats on a low Na diet in the absence of renal and adrenal tissue. Moreover, in these normal kidneys, perfusion with 'S' blood induced a 16% higher renal vascular resistance than perfusion with 'R' blood (p less than 0.01), indicating vasoconstricting agents in 'S' blood. However, the Na-retaining humoral effect in 'S' blood could lead to Na retention by 'S' kidneys in vivo, which could partially account for the susceptibility of 'S' rats to NaCl hypertension. Hypertension in Dahl 'S' rats can be almost completely prevented by concomitant treatment with thiazide diuretics which act mainly on the kidney to facilitate Na excretion. This result is in agreement with the hypothesis that a shift in the pressure natriuresis curve, reducing Na excretion for a given arterial pressure, is partially responsible for the great sensitivity to NaCl hypertension in the 'S' rat. The Na-retaining hormone may contribute to this shift.

Animals↗
PubMed1978

Central nervous system pressor responses in rats susceptible and resistant to sodium chloride hypertension.

1. The pressor responses to hypertonic saline and angiotensin II introduced into the left lateral ventricle were both significantly greater in salt-sensitive (S) rats compared with salt-resistant (R) rats, with all rats on a low Na diet. 2. When S rats were given thiazide to nullify the pressor effect of dietary NaCl, their blood pressure averaged only 5 mmHg higher than that of the R rats; nevertheless, these S rats had significantly higher central nervous system pressor responses to angiotensin II and hypertonic saline. 3. Thus, if excessive dietary Na increases blood pressure by way of action on the central nervous system, these heightened pressor responses could partially account for the NaCl hypertension in S rats. Alternatively, depressed central nervous system pressor responses in R rats could partially explain the resistance of R rats to NaCl hypertension.

Angiotensin II↗
PubMed1978

A new, simple test for renin sampling.

In 8 of 18 patients with suspected diagnosis of renovascular hypertension, the resting renin values were inconclusive. However, following tourniquet stress, the values became positive. Sixteen of 18 patients showed significant decrease in blood pressure following surgery. The procedure was well tolerated, and its routine use is recommended.

Adolescent↗
PubMed1977

Evidence that prostaglandin synthesis inhibitors increase the concentration of sodium and chloride in rat renal medulla.

Thirty minutes after indomethacin (10 mg/kg, iv), a prostaglandin synthesis inhibitor, had been given to 10 rats, the Na concentration in renal papilla averaged 349 mEq/kg H2O, whereas it averaged only 181 in 14 "non-indomethacin" control rats (P less than 0.0001). Papillary plasma flow was closely similar in both groups. In a subsequent study, eight "indomethacin" rats had the same papillary flow as seven non-indomethacin rats but had a papillary Na concentration of 358 vs. 185 in the non-indomethacin controls (P less than 0.0001). In nine more rats, indomethacin increased Cl concentration in papillas by 66% (P less than 0.0001), while Na concentration increased 60% (P less than 0.0001). In eight other rats, micropuncture indicated that indomethacin does not greatly alter delivery of fluid out of late proximal tubule. Meclofenamate, another inhibitor, increased papillary Na just as much as indomethacin. Papillary urea is not changed with indomethacin. Thus, papillary Na concentration was almost twice as high in indomethacin rats, despite similar papillary plasma flow and late proximal flow. Apparently, inhibiting prostaglandin synthesis is associated with either a great increase in Na or Cl "pumping" or a great decrease in Na or Cl "leak" in either collecting duct or ascending limb, or in both. The collecting duct and papillary interstitial cells both synthesize prostaglandins, which seem to have a profound effect on medullary net Na transport.

Animals↗
PubMed1976

Low renal papillary plasma flow in both Dahl and Kyoto rats with spontaneous hypertension.

Abnormally low plasma flow to renal papilla characterizes Dahl hypertension. When eating a normal Na diet (0.3% NaCl) both hypertension-sensitive (S) rats and hypertension-resistant (R) rats, 16 weeks old, have fairly normal blood pressure (BP), averaging 144 and 129 mm Hg, respectively. However, even in this barely hypertensive state, 18 S rats had a 31% lower papillary plasma flow (Lilienfield method) than 22 R rats, 19.2 ml/100 g of papilla per min compared to 25.6 (P less than 0.001). When a high (8%) NaCl diet was fed for 7 days, R rats increased papillary plasma flow from 25.6 on 0.3% NaCl to 33.8 on 8% NaCl, a 32% rise (P less than 0.001). S rats increased papillary flow from 20.4 to 24.8, a 22% rise (P less than 0.05). When a high (8%) NaCl diet was fed for 4 weeks, R rats increased papillary plasma flow from 25.7 ml/100 g per min on 0.3% NaCl to 29.5 ml/100 g per min on 8% NaCl, a 15% rise (P less than 0.025). S rats increased papillary flow from 17.7 to 20.0 ml/100 g per min (not significant). S rats on 8% NaCl had a papillary flow 32% lower than R rats on 8% NaCl (P less than 0.001). BP of S rats rose to 162 mm Hg after 4 weeks on 8% NaCl; in R rats, BP did not rise at all. S rats on 0.3% NaCl have a low papillary flow even in a borderline hypertensive state. When challenged with 8% NaCl, R rats increased papillary flow, an adaptation possibly important for the natriuresis. S rats failed to achieve this same high papillary flow. Lacking this adaptation, hypertension may then conceivably occur in S rats to accomplish natriuresis through a "pressure natriuresis" mechanism. Papillary flow also decreased by 11% in 26 Kyoto 17-week-old spontaneously hypertensives (BP, 182 mm Hg) compared to 24 Kyoto normotensives (BP, 118 mm Hg), 29.5 vs 33.2 ml/100 g per min (P less than 0.001). Thus, low papillary flow exists in both hypertensions.

Animals↗