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Biomedical subjects

L Tobian

Publications and source records attributed to L Tobian.

At least 55 records · Page 3Linked to original sources
PubMed1986

Platelet thromboxane inhibition by plasma polypeptides in prehypertensive Dahl rats.

Plasma from Dahl rats susceptible to salt-induced hypertension (Dahl S rats) contains inhibitory factors that reduce the release of thromboxane A2 from thrombin-activated platelets. Platelet-rich plasma from Dahl S rats on either low salt (0.11 or 0.3% NaCl) or high salt (4% NaCl) diets released about 50% less thromboxane A2 than comparable plasma from Dahl rats that are resistant to hypertension (Dahl R rats). This inhibitory activity was present even in the blood of 4-week-old completely normotensive Dahl S rats on a diet containing 0.11% low NaCl. The inhibitory activity could be transmitted to platelets of normal Sprague-Dawley rats by incubating these platelets in boiled and dialyzed plasma from Dahl S rats. Moreover, the inhibitory activity could be completely washed off the Dahl S platelets by incubation in Dahl R plasma. Thus, Dahl S plasma contains inhibitory factors that reduce platelet thromboxane A2 release. The factors are found in low concentrations even in Dahl R plasma; and in Dahl S or Dahl R plasma the factors are increased 25 to 32% by a 4% high NaCl diet. Digestion of Dahl S and Dahl R plasma with either trypsin or chymotrypsin destroyed the inhibitory factors, which have a molecular weight between 2,000 and 3,500. Twenty-four hours after bilateral nephrectomy, dialyzed plasma from both Dahl S and Dahl R rats was completely devoid of thromboxane A2 inhibitory activity. Thus, the factors appear to be heat-stable polypeptides either produced in the kidney or greatly influenced by the presence of renal tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

High-potassium diets markedly protect against stroke deaths and kidney disease in hypertensive rats, an echo from prehistoric days.

Male stroke prone spontaneously hypertensive rats (SHRSP) were fed 4% NaCl diet containing either 0.75% normal potassium or 2.11% high-potassium, starting at 6 weeks of age. After 8 months on these diets, 40 out of 58 SHRSP on 0.75% potassium had died (69% mortality) versus two dead out of 95 on 2.11% potassium (2% mortality), a 97% reduction in mortality, P less than 0.000 01. After 20 weeks on the diet, the daytime and night-time blood pressures (BPs) of each rat were measured intra-arterially under light ether. Using these accurate BPs, we selected two groups precisely matched for BP. One matched SHRSP group (BP 182) ate the 0.75% potassium diet and 30 out of 47 rats died (64% mortality). The other matched SHRSP group (BP 182) ate the 2.11% potassium diet and two out of 35 died (6% mortality) a 91% reduction of mortality, P less than 0.0001. Seemingly, the striking reduction in mortality rate with the 2.11% high-potassium diet does not depend on a lowering of BP. High-potassium diets do not change muscle, aorta or body sodium or potassium. Dry weight of mesenteric arterioles was reduced 29% on the 2.11% potassium diet versus the 0.75% potassium diet [5.43 mg versus 7.66 mg] (P less than 0.0001) indicating a greatly reduced hypertensive hypertrophy, even though BP was equal in the two groups being compared. Aortic wall wet weight was reduced 25.5% in 36 rats on a 2.11% potassium diet versus 26 rats on a 0.75% potassium diet (36.7 mg versus 49.2 mg) P less than 0.001, even though BP was equal in the two groups being compared. In nine surviving SHRSP rats on 0.75% potassium, 13 of 36 brain hemisphere slides (four slides per rat) showed infarcts (36%). In 11 surviving SHRSP rats on 2.11% potassium, one of 44 brain slides showed infarcts (2%, a 95% reduction) P less than 0.0001. In other SHRSP rats on a 0.75% diet for 8 weeks, 18 of 25 rats (72%) had spots of brain haemorrhages whereas only two of 36 rats (5.5%) on 2.11% potassium had similar haemorrhages - a 92% reduction (P less than 0.000 01). High-potassium diets allow cerebral arteries to carry very high BPs without sustaining damage to the artery wall, thereby drastically reducing brain haemorrhages and infarcts and lowering the death rate. Moreover, hypertension does not invariably lead to artery hypertrophy, since a high-potassium diet can prevent most of it.

Animals↗
PubMed1986

Reduction of blood pressure in salt-fed Dahl salt-sensitive rats with diets rich in olive oil, safflower oil or calcium biphosphate but not with calcium carbonate.

Increased dietary calcium as CaCO3 had no effect in NaCl-induced hypertension in Dahl salt-sensitive (Dahl-S) rats, while the calcium supplementation as CaHPO4 did lower the blood pressure (BP). A diet rich in either monounsaturated or polyunsaturated fatty acids produced a significant lowering of blood pressure compared with the relatively saturated palm-oil diet in NaCl-induced hypertension in Dahl-S rats. The lower BP found with olive oil is probably not related to increased amounts of PGE2 and PGI2.

Animals↗
PubMed1986

High-K diets reduce brain haemorrhage and infarcts, death rate and mesenteric arteriolar hypertrophy in stroke-prone spontaneously hypertensive rats.

Male stroke-prone spontaneously hypertensive rats (SHRSP) were fed 4% NaCl diets containing either 0.75% normal K or 2.11% high K, starting at 6 weeks of age. After 8 months on these diets 69% of 58 SHRSP rats on 0.75% K had died, whereas 2% of 95 rats of 2.11% K died, a 98% reduction in mortality, P less than 0.000 001. After 20 weeks the daytime and night-time blood pressure (BP) of each rat were measured intra-arterially. We selected two groups precisely matched for BP. One matched SHRSP group (BP 182 mmHg) ate the 0.75% K diet and 30 of 47 rats died (64% mortality). The other matched SHRSP group (BP 182 mmHg) ate the 2.11% K diet, and two of 35 died (6% mortality, a 91% reduction of mortality, P less than 0.0001). Seemingly, the striking reduction in mortality rate with the 2.11% hig-K diet does not depend on a lowering of BP. High-K diets do not change body Na or K. The dry weight of mesenteric arterioles was reduced by 22% on 2.11% K diet versus 75% K (7.5 versus 9.7 mg) (P less than 0.001), indicating a greatly reduced hypertensive hypertrophy. In nine surviving SHRSP on 0.75% K, 13 of 36 brain hemisphere slides (four slides per rat) showed infarcts (36%). In 11 surviving SHRSP on 2.11% K, one of 44 brain slides showed infarcts (2%, a 94.5% reduction, P less than 0.0001). Brain haemorrhage was reduced by 92% on the 2.11% K diet. High-K diets allow cerebral arteries to carry very high BPs without sustaining damage to the artery wall, thereby drastically reducing brain infarcts and lowering the death rate.

Animals↗
PubMed1985

Prostaglandin alterations in barely hypertensive Dahl S rats.

In summary, prostacyclin, PGE2, and PGD2 are vasodilators and had significantly lower renal cortical and outer medullary concentrations in the borderline hypertensive S rats compared to normotensive R rats. Conversely, thromboxane is a vasoconstrictor which had significantly higher renal cortical and outer medullary concentrations in borderline hypertensive S rats compared to normotensive R rats. Thus, in borderline hypertensive S rats, both renal cortex and outer medulla have a prostaglandin pattern which favors vasoconstriction in cortical vessels and in descending vasa recta. This could partially account for the increased renal vascular resistance and low papillary plasma flows which are integral components of Dahl hypertension. The low PGE2 in S kidneys would also enhance Na reabsorption in collecting tubules and ascending limbs, thereby encouraging Na retention and hypertension.

Animals↗
PubMed1984

Renal vein renin sampling in essential hypertension using hydralazine and the tourniquet test.

The results of renal vein renin sampling were assessed in 40 patients who had uncomplicated essential hypertension. All had normal creatinine clearance, intravenous pyelography, and arteriography. During sampling, renin release was stimulated in 29 patients with intravenous hydralazine and in 11 with the tourniquet blood trapping test. Simultaneous sequential renal vein samples were drawn over a 30-minute period. Positive renal vein renin ratios (greater than or equal to 1.5) were seen in 52% of the hydralazine group at 0 minutes and in 69% post-hydralazine. In the tourniquet group, 27% had a positive ratio at 0 minutes as compared with 64% post-tourniquets. A significant difference was found in renal vein plasma renin activity between the two kidneys (p greater than or equal to .0001). The asymmetry of renal vein renin activity and the large renal vein renin ratios in these two groups suggest the presence of true differences in renin secretion. These differences may be due to focal nephrosclerosis. The therapeutic significance of a positive renal vein renin ratio in the hypertensive patient should be determined in conjunction with arteriography.

Blood Volume↗
PubMed1984

Potassium prevents death from strokes in hypertensive rats without lowering blood pressure.

Adding potassium to normal chow reduces death rate in hypertensive stroke-prone (SHRSP) rats from 83 to 2%, a 98% reduction. An 86% reduction in deaths occurred even when blood pressure (BP) was virtually equal in the two SHRSP groups being compared. Potassium supplements in the diet also reduced stroke deaths in hypertensive Dahl S rats from 55 to 4%, a 93% reduction. There was an 87% reduction in deaths even when BP was actually equal in the two Dahl S groups being compared. The added potassium in the diets decreased BP moderately in SHRSP rats and modestly in Dahl S rats, which contributed somewhat to the reduction in strokes. However, more importantly, the added potassium seems to reduce the intrinsic susceptibility to cerebral artery lesions for a given level of hypertension, even when BP is not lowered.

Animals↗
PubMed1983

Hydralazine and the tourniquet test in renal vein renin sampling: a comparison.

A total of 36 salt-depleted patients with suspected renovascular hypertension received intravenous hydralazine and 36 were subjected to the tourniquet test at the time of renal vein renin sampling. Simultaneous bilateral renal vein samples were obtained sequentially over 30 minutes. Both measures resulted in an increase in renin secretion. The number of patients showing a positive ratio (greater than or equal to 1.5) between the angiographically abnormal kidney and the contralateral kidney increased in both groups. In the hydralazine group, 47% had positive ratios at 0 min compared with 80% following hydralazine administration. In the tourniquet group, 53% had positive ratios at 0 min compared with 78% afterward. In neither group did all patients have positive ratios throughout the entire sampling period. Hydralazine produced a greater increase in renin, but more variable results. It is concluded that salt depletion is inadequate for detection of a pressor kidney, and an additional stress is required. Multiple simultaneous samples should be obtained.

Blood Pressure↗
PubMed1983

Human essential hypertension: implications of animal studies.

Hypertension has been linked to dietary sodium intake in humans. It is possible that 9% to 20% of the population may be genetically susceptible to developing essential hypertension by middle life. The remainder of the population may be genetically resistant to developing essential hypertension. A person genetically resistant to hypertension can ingest as much as 200 meq/d of salt without developing elevated blood pressure. However, in persons genetically susceptible to hypertension, a lifelong restriction of salt intake of less than 60 meq/d in adults may prevent hypertension indefinitely, and subsequent hypertensive complications. The same restriction of salt enhances the effect of most antihypertensive drugs and is the only treatment necessary in some persons with mild or moderate hypertension, especially the elderly.

Animals↗
PubMed1982

Effect of an anteroventral third ventricle lesion on NaCl hypertension in Dahl salt-sensitive rats.

An anteroventral third ventricle (AV3V) lesion in the brain prevents several forms of experimental hypertension. The present experiment was designed to determine whether the AV3V lesion prevents NaCl-induced hypertension in Dahl salt-sensitive (S) rats and whether attenuation of vasopressin release reported in lesioned rats contributes to the protective effect of the AV3V lesion against hypertension. After the AV3V lesion Dahl S rats received daily injections of either vasopressin (pitressin tannate, 500 mU/kg) or vehicle during 10 wk of 8% high-NaCl diet. Sham-lesioned rats served as controls. The blood pressure in sham-lesioned rats receiving vehicle was 189 mmHg after 10 wk of high-NaCl diet. Lesioned rats given vehicle showed a significantly smaller increase in blood pressure than sham-lesioned rats (P less than 0.001), the blood pressure averaging 161 mmHg at 10 wk. Lesioned rats given vasopressin also showed a smaller increase in blood pressure than sham-lesioned rats (P less than 0.05), but the final blood pressure averaged 176 mmHg and was significantly higher than that of lesioned rats given vehicle (P less than 0.025). Vasopressin injections corrected the hypernatremia in lesioned rats. In another experiment the effect of the AV3V lesion on the renal papillary plasma flow (RPPF) in Dahl S rats was studied. Dahl S rats have a lower RPPF than Dahl salt-resistant (R) rats even on a low-NaCl intake. The AV3V lesion increased the RPPF by 14% in S rats (P less than 0.025). These findings suggest that NaCl-induced hypertension in Dahl S rats requires the integrity of the AV3V region for its full expression, and the ability of the AV3V lesion to attenuate the NaCl-induced hypertension in Dahl S rats is partly related to the attenuation of vasopressin release. Moreover, the AV3V lesion partly corrected one of the characteristic features of Dahl S rats, the reduction in RPPF, when compared with Dahl R rats, with both strains on a low-NaCl intake.

Animals↗
PubMed1981

Brain lesions in the paraventricular nuclei and catecholaminergic neurons minimize salt hypertension in Dahl salt-sensitive rats.

1. The rise in blood pressure in Dahl salt-sensitive rats that received intracerebroventricular 6-hydroxydopamine was almost half that of the control rats throughout 20 weeks of high (8%) NaCl feeding. 2. The rise in blood pressure in Dahl salt-sensitive rats with bilateral complete electrolytic lesions of the paraventricular nuclei was almost half that of the control rats during 12 weeks of high (8%) NaCl feeding. 3. The bilateral complete electrolytic lesions of the suprachiasmatic nuclei enhanced the development of NaCl hypertension in Dahl salt-sensitive rats. 4. These results show that NaCl-induced hypertension in Dahl salt-sensitive rats requires the integrity of the central nervous system catecholaminergic neurones and the paraventricular nuclei for its full expression.

Animals↗