Ca fluxes across duodenum and colon of spontaneously hypertensive rats: effect of 1,25(OH)2D3

1986 ◽  
Vol 251 (2) ◽  
pp. F278-F282 ◽  
Author(s):  
U. Gafter ◽  
S. Kathpalia ◽  
D. Zikos ◽  
K. Lau
Keyword(s):  
Calcium Transport ◽  
Spontaneously Hypertensive Rats ◽  
Calcium Absorption ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Calcium Flux ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto

Calcium absorption by spontaneously hypertensive rats (SHR) was variably reported to be different from normotensive Wistar-Kyoto (WKY) controls. Furthermore, blunted responsiveness to the intestinal effects of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] has also been postulated. To evaluate this hypothesis, calcium fluxes were measured by the Ussing technique across duodenum and descending colon with or without prior 1,25(OH)2D3 treatment. Duodenal mucosal-to-serosal calcium flux (Jm----s) (44.9 vs. 52.4 nmol X cm-2 X h-1), serosal-to-mucosal flux (Js----m) (25.6 vs. 28.4 nmol X cm-2 X h-1), and net flux (Jnet) were comparable. 1,25(OH)2D3 increased duodenal Jm----s in both SHR and WKY groups (95.2 and 86.8 nmol X cm-2 X h-1). Js----m was lower in SHR (26.1 vs. 35.6 nmol X cm-2 X h-1, P less than 0.01), although the tendency for a higher Jnet in SHR (68.6 vs. 51.2 nmoles X cm-2 X h-1) was statistically insignificant. Short-circuit current was higher in the colon of SHR, both before and after 1,25(OH)2D3, suggesting increased sodium transport. Basal colonic Jnet was virtually zero in both groups but comparably increased by 1,25(OH)2D3 because of stimulation in only Jm----s. Prevention of hypertension by hydralazine since the 4th wk of age did not alter the findings compared with the hypertensive SHR, suggesting calcium transport rates were unaffected by hypertension. These data indicate that in vitro, duodenal, and colonic active calcium transport by the SHR is similar to WKY. Their normal responses to 1,25(OH)2D3 do not support the hypothesis of intestinal resistance.

Myogenic tone in mesenteric arteries from spontaneously hypertensive rats

1996 ◽  
Vol 270 (1) ◽  
pp. H1-H6 ◽  
Author(s):  
A. S. Izzard ◽  
S. J. Bund ◽  
A. M. Heagerty
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Mesenteric Arteries ◽  
Myogenic Tone ◽  
Hypertensive Rats ◽  
Tension Development ◽  
Spontaneously Hypertensive ◽  
Wide Pressure Range ◽  
Wistar Kyoto ◽  
Wide Pressure

To investigate myogenic tone during the developmental and established phases of hypertension, segments of distal (6th order) mesenteric arteries from spontaneously hypertensive rats (SHR) at 5 and 20 wk were isolated and pressurized in vitro and compared with vessels from age-matched Wistar-Kyoto (WKY) control animals. At 5 wk, tone was significantly enhanced in the SHR. At 20 wk tone was no longer significantly increased over a wide pressure range, although arteries from the SHR were able to maintain diameter at all pressures studied, whereas vessels from the WKY exhibited forced distension at 180 and 200 mmHg. From the relative slope of the pressure-diameter relationship (myogenic index), no increase in peak myogenic responsiveness was observed in arteries from the SHR at either time point. Passive lumen diameters were significantly decreased in arteries from SHR at both time points. From the total and passive midwall circumference-tension relationships, total tension was observed at a reduced midwall circumference in the SHR, but increased absolute levels of total tension were not observed. The normalized midwall circumference-tension relationships in the two strains revealed increased total tension due to active tension development at a reduced normalized circumference at 5 wk in the SHR. At 20 wk the normalized midwall circumference-tension relationships in the two strains were identical. These results demonstrate that myogenic tone in mesenteric arteries is enhanced during the development of hypertension but not when it is established, except at high intraluminal pressures.

Decreased in vitro responses to vasoconstrictors during gestation in normotensive and spontaneously hypertensive rats

1987 ◽  
Vol 65 (12) ◽  
pp. 2466-2471 ◽  
Author(s):  
G. Massicotte ◽  
J. St-Louis ◽  
A. Parent ◽  
E. L. Schiffrin
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Female Rats ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Response Curves ◽  
Pregnant Rats ◽  
Spontaneously Hypertensive ◽  
Vasoconstrictor Agents ◽  
Wistar Kyoto

We have investigated the in vitro vascular responses to vasoconstrictor agents in pregnant normotensive (Sprague–Dawley (SDR) and Wistar–Kyoto (WKR)) and spontaneously hypertensive rats (SHR) to measure the sensitivity and contractility of blood vessels of pregnant rats. In the perfused mesenteric vascular bed from rats on the 21st day of gestation, the concentration–response curves for the increase in perfusion pressure by arginine8-vasopressin and norepinephrine were displaced to the right by comparison to nonpregnant female rats when all strains of rats were considered together. The increase in EC50 to both agents in pregnant rats was from 1.3- to 2.7-fold in the mesenteric bed; SDR showed the highest increase in EC50, followed by SHR and WKR. No consistent effect was observed on the maximum response. Similar results were obtained in isolated portal veins for angiotensin II and norepinephrine, except that the increase in EC50 in pregnant rats was smaller in magnitude (from 1.0 to 1.7) and followed the same interstrain pattern. These data show that the decreased responsiveness to vasoconstrictor agents in pregnant rats observed in vitro is similar in normotensive and hypertensive rats and suggest that the factor(s) responsible for this effect is a phenomenon affecting vascular smooth muscle in both arteries and veins.

Norepinephrine effect on in situ venous membrane potential in spontaneously hypertensive rats

1981 ◽  
Vol 240 (6) ◽  
pp. H837-H842 ◽  
Author(s):  
D. R. Harder ◽  
S. J. Contney ◽  
W. J. Willems ◽  
W. J. Stekiel
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Physiological Salt Solution ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
In Vitro Measurements ◽  
The Mean ◽  
Wistar Kyoto ◽  
Made In

Comparative in situ (innervation and circulation intact) and in vitro measurements of transmembrane potential (Em) were made in vascular smooth muscle cells (VSM) of small (300-500 micrometers) veins of an externalized intestinal mesenteric loop in 13- to 15-wk-old anesthetized spontaneously hypertensive rats (SHR) and Wistar-Kyoto normotensive controls (WKY). During suffusion with physiological salt solution (PSS), the mean in situ Em in SHR was significantly lower (-34 +/- 0.8 mV) than in WKY (-49 +/- 1.3 mV). In situ neural blockade with 1 microgram/ml tetrodotoxin (TTX) in PSS hyperpolarized venous Em in SHR (-45 +/- 1.7 mV) but not in WKY. In vitro Em in SHR (-51 +/- 1.0 mV) and WKY (-54 +/- 1.1 mV), though significantly elevated above respective in situ values, did not differ significantly from each other and were not altered by TTX. Increasing norepinephrine (NE) concentrations in the PSS gradedly depolarized the venous VSM of WKY in situ to a plateau Em of -32 +/- 0.9 mV at 6 microM (1 micrograms/ml) NE but had no significant depolarizing effect on the less-polarized venous VSM of SHR. However, after addition of 1 micrograms/ml TTX to the PSS, the in situ Em in SHR followed a depolarizing NE dose-response curve similar to that observed in WKY (with or without TTX). These results support the hypothesis that the neurogenic vasoconstrictor component of VSM tone is significantly elevated in mesenteric veins of the SHR model of essential hypertension.

Proton efflux from rat skeletal muscle in vivo: changes in hypertension

1992 ◽  
Vol 82 (5) ◽  
pp. 489-491 ◽  
Author(s):  
G. J. Kemp ◽  
C. H. Thompson ◽  
G. K. Radda
Keyword(s):  
Skeletal Muscle ◽  
Intracellular Ph ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Proton Efflux ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Wistar Kyoto

1. An analysis of the recovery kinetics of intracellular pH and phosphocreatine concentration after exercise in skeletal muscle was developed to calculate the rate of proton efflux in vivo. 2. Recovery of rat leg muscle pH after sciatic nerve stimulation was faster in spontaneously hypertensive rats than in Wistar-Kyoto controls (both n = 5). 3. Analysis of these data showed that the rate of proton efflux depends on intracellular pH, being greater at lower pH. 4. The early rate of proton efflux was greater in spontaneously hypertensive rats [measured over the first 0.8 min, 12.5 mmol min−1 kg−1 (sem 1.8) in spontaneously hypertensive rats compared with 7.6 mmol min−1 kg−1 (sem 0.4) in Wistar-Kyoto rats, P < 0.05], even though pH at the start of recovery was higher [6.30 (sem 0.03) in spontaneously hypertensive rats compared with 6.17 (sem 0.01) in Wistar-Kyoto rats, P < 0.01]. 5. This novel analysis provides a quantitative estimate of the rate of proton efflux in vivo, and demonstrates directly that this is increased in spontaneously hypertensive rats, as has previously been inferred from pH changes during exercise and studies of cultured muscle cells in vitro.

scholarly journals Spinal and peripheral mechanisms contributing to hyperactive voiding in spontaneously hypertensive rats

1998 ◽  
Vol 275 (4) ◽  
pp. R1366-R1373 ◽  
Author(s):  
Katarina Persson ◽  
Raj K. Pandita ◽  
John M. Spitsbergen ◽  
William D. Steers ◽  
Jeremy B. Tuttle ◽  
...  
Keyword(s):  
Marked Reduction ◽  
Spontaneously Hypertensive Rats ◽  
Electrical Field Stimulation ◽  
Bladder Function ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Wistar Kyoto

The influence of noradrenergic mechanisms involved in micturition in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats was investigated using continuous cystometry in in vivo and in vitro studies on isolated bladder and urethral tissues. Compared with WKY rats, SHR had a significantly lower bladder capacity (SHR: 0.7 ± 0.05 ml; WKY rats: 1.3 ± 0.06 ml; P < 0.001), micturition volume (SHR: 0.4 ± 0.04 ml, WKY rats: 1.2 ± 0.05 ml; P < 0.001), and an increased amplitude of nonvoiding (unstable) bladder contractions. The effects of intrathecal and intra-arterial doxazosin on cystometric parameters were more pronounced in SHR than in WKY rats. There was a marked reduction in nonvoiding contractions after intrathecal (but not intra-arterial) doxazosin in SHR. Norepinephrine (0.1 μM–1 mM) failed to evoke contractions in bladder strips from WKY rats, in contrast to a weak contractile response in SHR. The response to electrical field stimulation was significantly less in bladder strips from SHR than from WKY rats. In WKY rats, norepinephrine produced concentration-dependent inhibition (87 ± 5%, n = 6) of nerve-evoked bladder contractions. Almost no inhibition (11 ± 8%, n = 6) was found in SHR. Alterations in bladder function of SHR appear to be associated with changes in the noradrenergic control of the micturition reflex, in addition to an increased smooth muscle and decreased neuronal responsiveness to norepinephrine. The marked reduction in nonvoiding contractions after intrathecal doxazosin suggests that the bladder hyperactivity in SHR has at least part of its origin in supraspinal and/or spinal structures.

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