Anesthesia and microvascular dynamics in spontaneously hypertensive rats

1981 ◽  
Vol 241 (6) ◽  
pp. H821-H828
Author(s):  
F. A. De Lano ◽  
B. W. Zweifach
Keyword(s):  
Blood Pressure ◽  
Systemic Blood Pressure ◽  
Vessel Diameter ◽  
Background Information ◽  
Unstable State ◽  
Sprague Dawley ◽  
Systemic Blood ◽  
Spontaneously Hypertensive ◽  
Anesthetic Agents ◽  
Wistar Kyoto

Studies on pressure dynamics in rats under local anesthesia were carried out to provide background information for subsequent intravital analysis of microvascular behavior in a skeletal muscle. An alpha-chloralose-urethan mixture (1:13.3%) was selected as the general anesthesia having the least effect on systemic pressures in spontaneous hypertensive (SHR) as well as normotensive (WKY), Sprague-Dawley and Wistar-Kyoto rats. Anesthetic agents, in general, lower systemic blood pressure in SHR by 30—50 mmHg and thereby distort microcirculatory flow and blood vessel-diameter relationships. Insertion of a plastic catheter into the trachea of the anesthetized rat, to maintain an open airway, had a complex effect on heart rate and systemic blood pressure and left the pressure in an unstable state. Severity of the change depended on the age of the rat and the anesthetic agent; hypertensive animals were especially vulnerable.

Effect of episodic eucapnic and hypocapnic hypoxia on systemic blood pressure in hypertension-prone rats

1996 ◽  
Vol 81 (5) ◽  
pp. 2088-2094 ◽  
Author(s):  
Eugene C. Fletcher ◽  
Gang Bao
Keyword(s):  
Blood Pressure ◽  
First Generation ◽  
Systemic Blood Pressure ◽  
Sprague Dawley ◽  
Systemic Blood ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Acute Response ◽  
Daytime Blood Pressure ◽  
Wistar Kyoto

Fletcher, Eugene C., and Gang Bao. Effect of episodic eucapnic and hypocapnic hypoxia on systemic blood pressure in hypertension-prone rats. J. Appl. Physiol. 81(5): 2088–2094, 1996.—Repetitive episodic (18–24 s twice per minute) hypocapnic hypoxia (HH) administered chronically (7 h/day, 35 days) to Sprague-Dawley or Wistar-Kyoto rats results in a sustained increase in daytime blood pressure (BP). We examined acute and chronic BP response to episodic HH and eucapnic hypoxia (EH) in borderline hypertensive rats [first generation (F1) cross between spontaneously hypertensive and Wistar-Kyoto rats]. We hypothesized that episodic HH and EH would create a greater increase in acute and chronic BP in this breed of rat than in previously studied strains. We also examined neural mechanisms by which BP changes from hypoxia are induced. BP and heart rate were examined acutely in nine F1 rats during baseline, HH, EH, EH with prazosin, and EH with prazosin and atropine. Five groups of male F1 rats were studied after 35-day exposure to the following: Unhandled ( n = 8): no treatment; Sham ( n = 10): episodic compressed air; HH ( n = 14): daily episodic hypoxia (2.7%); EH1 ( n = 12): hypoxia 2.9%, CO2 8.4%; and EH2 ( n = 11): hypoxia 2.8% and CO2 10.5%. Under acute conditions, HH caused a 34.2-mmHg and EH a 77.9-mmHg increase in mean BP. Prazosin partially blocked the increase in BP. Under chronic conditions, HH caused a 10.3-mmHg increase in daytime mean BP, whereas EH caused a fall in mean BP of 16.6 and 9.3 mmHg in the two separately studied groups. In the F1 rat, acute EH causes an elevation of BP but chronic EH causes a fall in BP. The acute response to EH is not predictive of what occurs after chronic exposure in the hypertension-prone F-1 rat.

Age-dependent overflow of endogenous norepinephrine from paraventricular hypothalamic nucleus of hypertensive rats

1993 ◽  
Vol 265 (1) ◽  
pp. H39-H46 ◽  
Author(s):  
J. M. Qualy ◽  
T. C. Westfall
Keyword(s):  
Blood Pressure ◽  
Neuronal Activity ◽  
Reciprocal Relationship ◽  
Hypothalamic Nucleus ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Paraventricular Hypothalamic Nucleus ◽  
Wistar Kyoto ◽  
The Relationship

The relationship between age and central noradrenergic neuronal activity of the paraventricular hypothalamic nucleus (PVH) was examined in 7- to 10-, 12- to 14-, and 30- to 36-wk-old Sprague-Dawley (SD), Wistar-Kyoto (WKY), and spontaneously hypertensive rats (SHR). As an index of noradrenergic activity, endogenous norepinephrine (NE) overflow was assessed utilizing a miniaturized push-pull cannula assembly in unanesthetized freely moving rats. NE overlow under basal, 56 mM K+ stimulation, and in response to pressor/depressor drugs, were examined in all three strains at all ages. Significant increases in basal and K(+)-stimulated overflow of endogenous NE from the PVH were observed in all ages of SHR compared with normotensive controls with the greatest percent increase occurring during the development of hypertension in SHR. In addition, a reciprocal relationship exists with respect to blood pressure and overflow of NE from the PVH such that increases/decreases in blood pressure elicit decreases/increases in NE overflow in all strains at all ages examined. However, developing hypertensive SHR exhibited attenuated decreases in overflow of NE from the PVH compared with age-matched controls and established hypertensive SHR. These results suggest that noradrenergic pathways of the PVH contribute to the development and maintenance of arterial pressure hemostasis and that enhanced central noradrenergic neuronal activity is greatest during the development of hypertension in SHR.

The vascular sensitizing character of plasma from spontaneously hypertensive rats

1981 ◽  
Vol 59 (11) ◽  
pp. 1111-1116 ◽  
Author(s):  
Gary L. Wright
Keyword(s):  
Blood Pressure ◽  
Plasma Levels ◽  
Spontaneously Hypertensive Rats ◽  
Vascular Tissue ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Tissue Sensitivity ◽  
Low Levels ◽  
Wistar Kyoto

Experiments were conducted to examine the effects of plasma from spontaneously hypertensive rats (systolic blood pressure (SBP) = 183 torr; 1 torr = 133.322 Pa) on the contractile properties of aortic strips from normotensive rats. While incubated in plasma from spontaneously hypertensive (SH) rats, the aortic strips of normotensive rats exhibited hyperresponsiveness to norepinephrine (NE) compared with those incubated in plasma obtained from Wistar–Kyoto (SBP = 128 torr) or Sprague–Dawley (SBP = 110 torr) rats. The washout of plasma and perfusion of the aortic strips with Krebs bicarbonate solution abolished the effect of SH plasma on the reactivity to NE but not potassium, suggesting a residual hypersensitivity. The comparison of these findings with results obtained for contractions of aortic strips in Krebs bicarbonate solution containing high and low levels of calcium indicated the effect of SH plasma on vascular tissue sensitivity was not directly related to an alteration in plasma levels of calcium.

scholarly journals Slowing down of chronic renal failure progression with captopril in spontaneously hypertensive rats with adriamycin nephropathy

2002 ◽  
Vol 130 (3-4) ◽  
pp. 73-80 ◽  
Author(s):  
Dijana Jovanovic ◽  
Djurdjica Jovovic ◽  
Jasmina Varagic ◽  
Jovan Dimitrijevic ◽  
Zorica Dragojlovic ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Early Stage ◽  
Systemic Blood Pressure ◽  
Hypertensive Rats ◽  
Systemic Blood ◽  
Spontaneously Hypertensive ◽  
Functional Changes ◽  
Slowing Down ◽  
Adriamycin Nephropathy

In SHRs with ADR nephropathy treatment with captopril normalized systemic blood pressure, and slowed down CRF progression in their early stage. These functional changes correlate with significant slowing of glomerular and interstitial changes.

Role of paraventricular nucleus in control of blood pressure and drinking in rats

1992 ◽  
Vol 262 (6) ◽  
pp. F1068-F1075 ◽  
Author(s):  
L. L. Jensen ◽  
J. W. Harding ◽  
J. W. Wright
Keyword(s):  
Blood Pressure ◽  
Paraventricular Nucleus ◽  
Critical Role ◽  
Systemic Blood Pressure ◽  
Dependent Manner ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Systemic Blood ◽  
Dose Dependent

The present investigation examined the abilities of angiotensin (ANG) II and III to produce increases in blood pressure and drinking when microinfused into the paraventricular nucleus (PVN) of the hypothalamus of the Sprague-Dawley rat. Dose-dependent elevations in systemic blood pressure and heart rate were measured to both ANG II and III in the anesthetized rat, with ANG II more potent than ANG III at the two highest doses examined. Pretreatment with the specific ANG receptor antagonist [Sar1,Thr8]ANG II (sarthran), blocked subsequent ANG II- and III-induced elevations in blood pressure, suggesting that these responses were dependent on the activation of ANG receptors. A similar analysis in awake rats yielded nearly equivalent results. A final experiment demonstrated that microinfusions of ANG II and III into the PVN produced drinking in a dose-dependent manner, with greater consumption to ANG II than ANG III. Again, sarthran was found to block the dipsogenic response. Histological examination revealed that the location of the injection site was linked to the character of the ANG-dependent response. These data suggest that the PVN may play a critical role in mediating central ANG effects on body water homeostasis and blood pressure regulation. Furthermore, it appears that subnuclei of the PVN may participate differentially in ANG-mediated actions.

Effects of endothelin 3 on diastolic blood pressure of pithed Sprague–Dawley, Wistar–Kyoto, and spontaneously hypertensive rats before and after pretreatment with nifedipine

1991 ◽  
Vol 69 (4) ◽  
pp. 531-535 ◽  
Author(s):  
Reza Tabrizchi ◽  
Christopher R. Triggle
Keyword(s):  
Blood Pressure ◽  
Calcium Channel ◽  
Diastolic Blood Pressure ◽  
Sprague Dawley ◽  
Spontaneously Hypertensive ◽  
Pithed Rats ◽  
Before And After ◽  
Blood Pressures ◽  
Wistar Kyoto ◽  
Endothelin 3

Pressor actions of endothelin 3 (ET3) were examined in pithed Sprague–Dawley (SD), Wistar-Kyoto (WKY), and spontaneously hypertensive (SH) rats before and after the administration of the calcium channel antagonist, nifedipine. Systolic and diastolic blood pressures were recorded via an intra-arterial catheter from sodium pentobarbital anaesthized rats prior to pithing. The systolic and diastolic blood pressures recorded from SH rats were significantly greater than those of SD and WKY rats; however, after pithing there were no significant differences between the diastolic blood pressures among the various strains. Administration of nifedipine significantly reduced the diastolic blood pressure of pithed rats to an equal extent in all three strains. The infusion of ET3 produced a dose-dependent increase in diastolic blood pressure of SD, WKY, and SH rats, but neither vascular sensitivity nor reactivity to ET3 was altered in SH rats. Nifedipine was more effective at inhibiting the vasoactive actions of ET3 in SD and WKY than in SH rats. It was therefore concluded that the pressor actions of ET3 in SH rats may be less dependent on the influx of calcium through a dihydropyridine-sensitive calcium channel as compared with WKY and SD rats.Key words: endothelin 3, calcium antagonist, diastolic blood pressure, spontaneously hypertensive, pithed rats.

Release of norepinephrine from the paraventricular hypothalamic nucleus of hypertensive rats

1988 ◽  
Vol 254 (5) ◽  
pp. H993-H1003 ◽  
Author(s):  
J. M. Qualy ◽  
T. C. Westfall
Keyword(s):  
Blood Pressure ◽  
Age Groups ◽  
Reciprocal Relationship ◽  
Hypothalamic Nucleus ◽  
Sprague Dawley ◽  
Spontaneously Hypertensive ◽  
Paraventricular Hypothalamic Nucleus ◽  
Arterial Blood ◽  
Freely Moving ◽  
Wistar Kyoto

The push-pull cannula was used to examine the release of endogenous norepinephrine (NE) from the paraventricular hypothalamic nucleus (PVH) of unanesthetized freely moving 7- to 10- and 12- to 14-wk-old Sprague-Dawley (SD), Wistar-Kyoto (WKY), and spontaneously hypertensive (SHR) rats. Basal NE release, K+ (56 mM) stimulation-induced NE release, and NE release in response to pressor/depressor drugs were examined in all three strains at both ages. Significant increases in basal and K+-stimulated release of endogenous NE from the PVH were observed in 7- to 10- and 12- to 14-wk-old SHR compared with the normotensive control rats suggesting that enhanced central noradrenergic nerve activity may be involved in the development and maintenance of hypertension in the SHR. In addition, a reciprocal relationship exists with respect to blood pressure and NE release from the PVH, i.e., decreases in blood pressure elicit increases in NE release, and increases in blood pressure elicit decreases in NE release in all three strains at both age groups, suggesting that the noradrenergic pathways of the PVH contribute to the maintenance of arterial blood pressure homeostasis.

Heme oxygenase substrates acutely lower blood pressure in hypertensive rats

1996 ◽  
Vol 271 (3) ◽  
pp. H1132-H1138 ◽  
Author(s):  
R. A. Johnson ◽  
M. Lavesa ◽  
K. DeSeyn ◽  
M. J. Scholer ◽  
A. Nasjletti
Keyword(s):  
Blood Pressure ◽  
Carbon Monoxide ◽  
Heme Oxygenase ◽  
Lower Blood Pressure ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Free Iron ◽  
Spontaneously Hypertensive ◽  
Lower Blood ◽  
Wistar Kyoto

Heme oxygenase catalyzes the metabolism of heme to biliverdine, free iron, and carbon monoxide. The current study was designed to determine if treatment with the heme oxygenase substrates heme-L-arginate or heme-L-lysinate, to stimulate formation of heme oxygenase products, can lower blood pressure in the rat. Heme-L-arginate (45 mumol/kg ip) and heme-L-lysinate (45 mumol/kg ip) acutely lowered blood pressure in awake spontaneously hypertensive rats (SHR) by approximately 35 mmHg. For both heme oxygenase substrates, this effect was blunted by pretreatment with an inhibitor of heme oxygenase, zinc deuteroporphyrin 2,4-bis glycol. Heme-L-lysinate also lowered arterial pressure in deoxycorticosterone acetate-salt hypertensive rats and in rats with phenylephrine-induced hypertension, indicating that the vasodepressive actions of heme may be extended to other hypertensive models. However, neither heme-L-arginate nor heme-L-lysinate decreased blood pressure in normotensive controls. The heme oxygenase product biliverdine did not lower blood pressure in SHR, and the vasodepressive actions of heme-L-lysinate were unaffected by pretreatment with deferoxamine to chelate free iron. Carbon monoxide (12 ml/kg ip) lowered blood pressure in SHR and in rats made hypertensive by phenylephrine infusion, had no effect on blood pressure in Wistar-Kyoto rats, and elicited only a modest vasodepressive response in normotensive Sprague-Dawley rats. We conclude that heme-bearing preparations can lower blood pressure in hypertensive rats, presumably via heme oxygenase-mediated formation of carbon monoxide.

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