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Biomedical subjects

L Tobian

Publications and source records attributed to L Tobian.

At least 109 records · Page 6Linked to original sources
PubMedDate not supplied

High potassium diets reduce macrophage adherence to the vascular wall in stroke-prone spontaneously hypertensive rats.

Our previous study demonstrated that high potassium (K) diets reduce stroke mortality in stroke-prone spontaneously hypertensive rats (SHRsp) even when the blood pressure is not lowered. On the other hand, macrophage infiltration into the vascular wall is known to play an important role in the development of arterial lesions. In this study, in vivo and in vitro experiments were performed to examine the effect of high K diets on macrophage adherence to the vascular wall in SHRsp rats. In the in vivo study, 51Cr-labelled macrophages, collected from the peritoneal cavity, were injected intravenously to SHRsp rats fed 6% high NaCl diets containing either normal 0.5% K or high 2.1% K, and, 45 min later, the rats were perfused with buffered saline to remove blood. Radioactivity from macrophages in the aorta was 40% lower in the high K SHRsp than in the normal K SHRsp (p < 0.002), and the brain of high K SHRsp also showed a 52% lower macrophage radioactivity than that of normal K SHRsp (p < 0.007). Although the mean blood pressure was slightly lower in the high K diet group than in the normal K diet group (167 vs. 184 mm Hg), these differences remained still prominent even when we compared groups with matching blood pressures; -33% for the aorta (p < 0.02) and -55% for the brain (p < 0.02). In the in vitro study, the aortas of SHRsp rats similarly fed on normal or high K diet were excised and mounted in a perfusion chamber. They were perfused with labelled macrophages at normotensive or hypertensive pressure. In normal K SHRsp, macrophage radioactivity remained in the washed aorta was 158% higher in high perfusion pressure group than in normal pressure (p < 0.002). However, they did not significantly differ between two perfusion pressures in high K SHRsp. These results indicate that high K diets reduce endothelial injuries which allow adherence and infiltration of macrophages into the vascular wall of hypertensive animals, and thereby contribute to the reduction of vascular lesions and stroke mortality.

Animals↗
PubMedDate not supplied

Cardiac output and peripheral resistance in strains of rats sensitive and resistant to NaCl hypertension.

The interrelationship of blood pressure, cardiac output, and peripheral resistance was studied in Dahl "S" and "R" rats after 3 days on a high (8%) NaCl diet. Both "S" and "R" rats were normotensive when fed a normal (0.3%) NaCl diet. After 3 days of the high NaCl diet, the "R" rats remained normotensive (BP 112 mm Hg), while the "S" rats had an elevation of arterial pressure (BP 133 mm Hg) (p less than 0.001). The cardiac outputs of both "S" and "R" rats were similar on the low NaCl diet. After 3 days of high NaCl feeding, the cardiac output of the "R" rats rose 18% above the "R" control level (p less than 0.0001), while the peripheral resistance declined 14% below the "R" control level (p less than 0.005), and the blood pressure (BP) did not change, a pattern quite contrary to the concept of "whole-body" autoregulation. With a similar 3-day high NaCl feeding in "S" rats, cardiac output (p less than 0.005) and peripheral resistance (p less than 0.05) both increased 10%, while BP rose 20%. After 7 days of high NaCl feeding, the cardiac output of the "S" rats had returned to normal, while blood pressure and peripheral resistance both continued to be elevated. This pattern of response in "S" rats could be compatible with the concept of "whole-body" autoregulation. However, since both NaCl hypertension and Goldblatt hypertension can occur in settings in which "whole-body" autoregulation appears not be to causally related, one cannot be certain whether "whole-body" autoregulation is playing a causal role in the mechanism of NaCl-induced hypertension in "S" rats. It is a striking dichotomy that 3 days of high salt feeding produces vasoconstriction in "S" rats and vasodilation in "R" rats.

Animals↗
PubMedDate not supplied

Potassium feeding reduces hyperactive central nervous system pressor responses in Dahl salt-sensitive rats.

Dahl showed that feeding KCl prevents the rise in blood pressure caused by a high NaCl diet in salt-sensitive Dahl "S" rats. Such S rats when normotensive on a low NaCl diet have a 2 to 3 times greater pressor response than Dahl "R" rats to intracerebroventricular hypertonic saline (600 mOsm/liter) or angiotensin II (AII) (500 ng). Does dietary KCl prevent NaCl hypertension in S rats partly by abolishing these hyperactive central nervous system (CNS) pressor responses? The effect of potassium-loading on CNS pressor responses was studied in S rats on a low (0.3%) NaCl diet. Drinking a 2% KCl solution reduced the CNS pressor responses in S rats to both AII and hypertonic saline by 44% (p less than 0.025) and brought them down almost as low as in R rats. KCl added to the low NaCl dry diet also decreased the CNS pressor responses in S rats to AII and to hypertonic saline by 39% (p less than 0.01) and 59% (p less than 0.02) respectively. K-citrate added to the low NaCl diet was generally as effective as KCl in reducing CNS pressor responses. K-citrate reduced the angiotensin pressor response by 44% (p less than 0.001) and the hypertonic saline pressor response by 46% (p less than 0.05). Thus, potassium feeding greatly diminished the hyperactive CNS pressor responses in S rats. This CNS action may well explain a good part of the protective effect of KCl against NaCl hypertension in S rats.

Angiotensin II↗
PubMedDate not supplied

A model of intervention for prevention of early essential hypertension in the 1980s.

The onset of essential hypertension early in life is indicated by the high tracking of blood pressure during adolescence; intervention in adults with mild hypertension has been found successful. How, then, can high blood pressure levels in children be modified to prevent early hypertensive cardiovascular disease in adulthood? In an entire biracial town (population 9000) we surveyed 1604 (89%) of all children aged 8--18 years for blood pressure and reexamined those in the upper decile of mean blood pressure (for each race, sex, and height) on three additional occasions. On each examination nine blood pressures were taken by trained observers. All children consistently in the top decile were randomly allocated into either a treatment (n = 50) or comparison (n = 50) group. These two groups and an additional midrange blood pressure comparison group (n = 50) were followed regularly using school facilities including community and school programs. Treatment consisted of 1) dietary guidance; 2) modifications of school lunches and snacks with healthy substitutes; 3) parental involvement; 4) a low dose diuretic and beta-antagonist given by usual standards. All study groups were monitored for blood pressure in a blind manner. In 6 months of observation, blood pressure in the treatment group remained 5 and 3 mm Hg (systolic and diastolic) less than controls (p less than 0.001 and p less than 0.01). An orchestrated community-wide attack on early-stage hypertension is feasible and seems to offer exciting potential for prevention of early hypertensive disease.

Adolescent↗
PubMedDate not supplied

Dahl S rats have increased natriuretic factor in atria but are markedly hyporesponsive to it.

Three experiments were carried out to determine whether atrial natriuretic factor (ANF) plays a part in Dahl hypertension. Results showed that ANF from both atria from 13 Dahl salt-sensitive (S) rats that had been fed a 4% NaCl diet for 12 weeks induced an average peak Na excretion of 23.0 muEq/min/g kidney in 13 Sprague-Dawley (SD) recipients vs 12.6 from atria from 13 salt-resistant (R) rats fed 4% NaCl (-45%, p less than 0.01), possibly indicating greater ANF secretion in S rats in order to enhance a reduced Na excretion. In 13 R rats, the ANF content in both atria increased from 14.0 after a 0.11% NaCl diet to 23.7 after 5 days of 4% NaCl diet (p less than 0.001) and then back to 12.6 after 12 weeks of 4% NaCl (p less than 0.001). Thus, ANF almost doubled after brief Na loading but returned to normal during continued Na loading. In S rats with a tendency to Na retention, ANF was elevated to about 23 in all three periods. ANF produced a 130-fold increase in natriuresis and a renal papillary plasma flow ( RPPF ) of 30.8 ml/min/100 g, 41% above the control level of 21.7, p less than 0.001. The marked increase in RPPF is very likely a partial cause of the natriuresis. A constant amount of ANF was continuously infused intravenously into 10 S rats and nine R rats all on 0.11% NaCl diets. Mean Na excretions in R and S were 5.3 and 4.6 muEq/min/100 g kidney before ANF.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗