Effects on Blood Pressure of Cross Circulation Between Spontaneously Hypertensive and Normotensive Rats

Zidek, Walter; Heckmann, U; Losse, H; Vetter, Hans

doi:10.3109/10641968609039609

Cited by 15 publications

(10 citation statements)

References 10 publications

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“…There was no significant difference between WKY blood and WKY blood with cytochalasin-D ( Figures 6D and 8A) although further study may be required using other microfilament blockers. In addition, blood exchange between WKY and SHR caused a significant increase in MABP in WKY ( Figure 8B), which is consistent with previous reports, 36 suggesting that pseudopod formation in SHR is in part responsible for the development of hypertension.…”

Section: Discussionsupporting

confidence: 92%

Contribution of Fluid Shear Response in Leukocytes to Hemodynamic Resistance in the Spontaneously Hypertensive Rat

Fukuda

Yasu

Kobayashi

et al. 2004

Circulation Research

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Abstract-The mechanisms for elevation of peripheral vascular resistance in spontaneously hypertensive rats (SHR), a glucocorticoid-dependent form of hypertension, are unresolved. An increase in hemodynamic resistance caused by circulating blood may be a factor. Physiological fluid shear stress induces a variety of responses in circulating leukocytes, including pseudopod retraction. Due to high rigidity, leukocytes with pseudopods have greater difficulty to pass through capillaries. Because SHR have more circulating leukocytes with pseudopods, we hypothesize that inhibition of the leukocyte shear response by glucocorticoids in SHR impairs normal leukocyte passage through capillaries and causes enhanced resistance in capillary channels. Fluid shear leads to retraction of pseudopods in normal leukocytes, whereas shear induces pseudopod projection in SHR and dexamethasone-treated Wistar rats.

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Section: Discussionsupporting

confidence: 92%

Contribution of Fluid Shear Response in Leukocytes to Hemodynamic Resistance in the Spontaneously Hypertensive Rat

Fukuda

Yasu

Kobayashi

et al. 2004

Circulation Research

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“…Both pro-and antihypertensive humoral factors which are known to circulate in the blood of spontaneously hypertensive rats [3,4] are able to modulate the arterial pressure by affecting the tone and reactivity of vessels. However, the mechanism of action of many humoral factors remains unclear, since the effects of nervous and humoral factors on the cardiovascular system are hard to distinguish in the whole organism.…”

Section: Abstract: Isolated Vessel; Humoral Factors; Electrical Stimmentioning

confidence: 99%

Humoral factor(s) circulating in the blood of spontaneously hypertensive rats increases vascular tone and reduces constrictive responses of isolated rat caudal artery to stimulation of sympathetic fibers of the vascular wall

Na¹,

Zharkova²,

Chuiko³

et al. 1996

Bull Exp Biol Med

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It is shown that the perfusion pressure in isolated rat caudal artery rises and constrictive responses to electrical stimulation decrease when the blood of normotensive Wistar-Kyoto rats perfusing the vessel was replaced by the blood of spontaneously hypertensive rats. The norepinephrine release from the sympathetic terminals is reduced. Key Words: isolated vessel; humoral factors; electrical stimulation; norepinephrine release; spontaneously hypertensive ratsBoth pro-and antihypertensive humoral factors which are known to circulate in the blood of spontaneously hypertensive rats [3,4] are able to modulate the arterial pressure by affecting the tone and reactivity of vessels. However, the mechanism of action of many humoral factors remains unclear, since the effects of nervous and humoral factors on the cardiovascular system are hard to distinguish in the whole organism.A new method we proposed previously, namely perfusion of an isolated segment of rat caudal artery with blood from a conscious donor rat, allowed us to study the humoral factors circulating in the blood of spontaneously hypertensive rats (SHR) and their influence on the constrictive responses to stimulation of sympathetic fibers in the vascular wall. A modification of this method supplemented by measurement of the norepinephrine (NE) release from presynaptic terminals of sympathetic fibers has en- MATERIALS AND METHODSThe experiments were carried out on 6-7-monthold normotensive Wistar-Kyoto rats (WKY) and SHR weighing 250-350 g. The animals were used as blood donors. To this end the rats were narcotized with Nembutal (40 mg/kg, intraperitoneally), and the carotid and femoral arteries and the femoral vein were catheterized. In the course of the experiment blood for perfusion of the isolated caudal artery was drawn by means of a roll pump through the catheter introduced in the carotid artery and returned to the donor through the catheter introduced in the femoral vein, and the arterial pressure and heart rate in the donor rats were recorded using the catheter implanted in the femoral artery. The animals were conscious and moved freely in the cage throughout the experiment.The isolated segments of the caudal artery were obtained from decapitated WKY. The segment

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“…In spontaneously hypertensive rats (SHR), a new approach to this problem was made with the observation that the parathyroid glands secrete a hypertensive factor [S], which is not found in the normotensive Wistar-Kyoto rats (WKY). In the Munster strain of SHR, hypertension could be transmitted to WKY by cross-circulation [9]. Therefore, in the present study, the chromatograpic characteristics and the isolation procedure of the underlying substance are described and compared with those of the 'parathyroid hypertensive factor' [lo].…”

mentioning

confidence: 99%

Partial purification and characterization of a circulating hypertensive factor in spontaneously hypertensive rats

Schlüter

Kluth

Börjesson‐Stoll

et al. 1993

European Journal of Biochemistry

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Parabiosis and cross-circulation experiments with spontaneously hypertensive and normotensive rats gave indicatiohs for a previously unidentified circulating hypertensive agent. In this study, plasma from normotensive and hypertensive rats was fractionated and the vasopressor action of the corresponding fractions was measured in the isolated perfused rat kidney. One of three vasoactive fractions obtained by gel filtration (Biol-Gel P2) from hypertensive rats showed a significantly higher activity (increase in perfusion pressure by 1502.9 2 438.9 Pa) than that from normotensive rats (increase in perfusion pressure by 505.4 ? 186.2 Pa, P < 0.01). Further chromatographic separations of this fraction revealed that the hypertensive factor is hydrophilic and has no ionic groups or vicinal diol groups. The molecular mass was estimated by dialysis and the matrix-assisted laser desorptiodionization mass spectrometry to be in the range of 1 kDa. The vasopressor is heat resistant and not degradable with trypsin or carboxypeptidase Y. The vasopressor action was not inhibited with the angiotensin-11-receptor antagonist saralasin, the a-receptor antagonist phentolamine, the thromboxane-receptor antagonist carbocyclic thromboxane A, or the serotonin antagonist ketanserine.The results confirm the existence of a vasopressor factor in the plasma of hypertensive rats and, in a lower concentration, of normotensive rats, which is possibly related to the pathogenesis of essential hypertension. The chromatographic behaviour suggests that this factor is different from the parathyroid hypertensive factor described recently.In primary hypertension, as yet unidentified circulating vasoconstrictor substances have long been postulated [l -61 ; recently, endogenous ouabain was isolated from human plasma [7]. In spontaneously hypertensive rats (SHR), a new approach to this problem was made with the observation that the parathyroid glands secrete a hypertensive factor [S], which is not found in the normotensive Wistar-Kyoto rats (WKY). In the Munster strain of SHR, hypertension could be transmitted to WKY by cross-circulation [9]. Therefore, in the present study, the chromatograpic characteristics and the isolation procedure of the underlying substance are described and compared with those of the 'parathyroid hypertensive factor' [lo]. It was found that our isolation procedure revealed a low-molecular-mass hydrophilic, non-peptide substance, which is not identical with the parathyroid hypertensive factor nor with ouabain. MATERIALS AND METHODS MaterialsBiol-Gel P2 (200-400-mesh, fine : Bio-Rad), norepinephrine hydrochloride, phentolamine hydrochloride, serotonin hydrochloride (5-hydroxytryptamine), angiotensin I1 acetate, carbocyclic thromboxane A, and the other agents used were purchased from Sigma, except the thromboxane receptor blocker, daltroban [ 11 -131, which was kindly provided by Boehringer Mannheim and ketanserin tartrate, a serotonin receptor blocker also inhibiting a,-adrenoceptors in high concentrations [14], which was supplie...

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Effects on Blood Pressure of Cross Circulation Between Spontaneously Hypertensive and Normotensive Rats

Cited by 15 publications

References 10 publications

Contribution of Fluid Shear Response in Leukocytes to Hemodynamic Resistance in the Spontaneously Hypertensive Rat

Contribution of Fluid Shear Response in Leukocytes to Hemodynamic Resistance in the Spontaneously Hypertensive Rat

Humoral factor(s) circulating in the blood of spontaneously hypertensive rats increases vascular tone and reduces constrictive responses of isolated rat caudal artery to stimulation of sympathetic fibers of the vascular wall

Partial purification and characterization of a circulating hypertensive factor in spontaneously hypertensive rats

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