Autonomic responses of the insular cortex in hypertensive and normotensive rats

1995 ◽  
Vol 268 (1) ◽  
pp. R214-R222 ◽  
Author(s):  
K. S. Butcher ◽  
D. F. Cechetto
Keyword(s):  
Wistar Rats ◽  
Spontaneously Hypertensive Rat ◽  
Focal Cerebral Ischemia ◽  
Insular Cortex ◽  
Cardiovascular Effects ◽  
Wistar Rat ◽  
Homocysteic Acid ◽  
Spontaneously Hypertensive ◽  
Pressor Responses ◽  
Acute Changes

Lesion and focal cerebral ischemia of the insular cortex (IC) results in elevated renal sympathetic nerve activity (RSNA) and arterial pressure (AP) in the Wistar rat, while the opposite effect is observed in the spontaneously hypertensive rat (SHR). Acute changes in AP, heart rate (HR) and RSNA were measured in propofol-anesthetized and conscious SHR (n = 17) and Wistar rats (n = 17) during pressure injection of D,L-homocysteic acid (DLH; 100 mM) and lidocaine (LID; 20 mg/ml) into the IC. DLH injections (200 nl) into the IC of anesthetized Wistar rats resulted in a significant increase in MAP (mean change = +27 +/- 7 mmHg; P < 0.05) and a significant decrease in HR (-22 +/- 9 beats/min) and RSNA (-11 +/- 4 microV.s). Neither DLH nor LID injections into the IC of anesthetized SHR affected MAP or RNA. DLH and LID injections (500 nl) into the IC of conscious Wistar rats both resulted in a significant increase in MAP (+26 +/- 5 mmHg; 11 +/- 4 mmHg, respectively). Neither DLH nor LID injections had any cardiovascular effects in the conscious SHR. It therefore appears that the IC of conscious Wistar rats has a tonic inhibitory output, while neural excitation is capable of eliciting pressor responses. Conversely, the IC of SHR appears to exert no tonic influence on MAP.

scholarly journals Thrombokinetic Study to Predict Epidodes of Thrombogenesis

1977 ◽  
Author(s):  
S. Koganemaru ◽  
Y. Taketomi ◽  
A. Kuramoto ◽  
K. Okamoto
Keyword(s):  
Blood Pressure ◽  
Animal Model ◽  
Cerebral Infarction ◽  
Intravenous Injection ◽  
Spontaneously Hypertensive Rat ◽  
Early Period ◽  
Wistar Rat ◽  
Spontaneously Hypertensive ◽  
Short Survival ◽  
Cerebrovascular Lesion

To evaluate platelet participation in the development of cerebrovascular lesion;cerebral infarction and / or bleeding in animal model, platelet survival and thrombopoiesis were measured by 75 Se-selenomethionine incorporation, using spontaneously hypertensive rat-stroke prone(SHR-SP. Okamoto-Yamori Strain). Our study on this newly established strain, was focused on the early period of life(5 and 10 weeks), when their blood pressure begin to increase above normal and spontaneous hypertension is established. Maximum peak of 75 Se-selenomethionine uptake into the platelets in circulation came on 3rd day after intravenous injection in SHR-SP as well as in controls(SHR-stroke resistant and normotensive Wistar rat). The value of incorporated activity in SHR-SP of 10 weeks with developing high blood pressure was significantly higher than those of 5 weeks and the controls. Expected survival obtained from the results by 75 Se-selenomethionine, suggested short survival of SHR-SP in 10 weeks of age, compared with the control. Short survival with increased turnover indicated increased consumption due to extrinsic moments, which might be brought about by vascular damage associated with the development of hypertension.

scholarly journals Genetic and Gender Influences on Sensitivity to Focal Cerebral Ischemia in the Stroke-Prone Spontaneously Hypertensive Rat

Hypertension ◽  
1999 ◽  
Vol 33 (2) ◽  
pp. 681-685 ◽  
Author(s):  
Hilary V. O. Carswell ◽  
Niall H. Anderson ◽  
James S. Clark ◽  
Delyth Graham ◽  
Baxter Jeffs ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Spontaneously Hypertensive Rat ◽  
Focal Cerebral Ischemia ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat ◽  
And Gender ◽  
Gender Influences

Postexercise hypotension in conscious SHR is attenuated by blockade of substance P receptors in NTS

2002 ◽  
Vol 283 (5) ◽  
pp. H1856-H1862 ◽  
Author(s):  
Chao-Yin Chen ◽  
Paul A. Munch ◽  
Anthony W. Quail ◽  
Ann C. Bonham
Keyword(s):  
Blood Pressure ◽  
Substance P ◽  
Nucleus Tractus Solitarius ◽  
Spontaneously Hypertensive Rat ◽  
Homocysteic Acid ◽  
Spontaneously Hypertensive ◽  
Afferent Fibers ◽  
Muscle Afferent ◽  
Postexercise Hypotension ◽  
Neurokinin 1

In hypertensive subjects, a single bout of dynamic exercise results in an immediate lowering of blood pressure back toward normal. This postexercise hypotension (PEH) also occurs in the spontaneously hypertensive rat (SHR). In both humans and SHRs, PEH features a decrease in sympathetic nerve discharge, suggesting the involvement of central nervous system pathways. Given that substance P is released in the nucleus tractus solitarius (NTS) by activation of baroreceptor and skeletal muscle afferent fibers during muscle contraction, we hypothesized that substance P acting at neurokinin-1 (NK-1) receptors in the NTS might contribute to PEH. We tested the hypothesis by determining, in conscious SHRs, whether NTS microinjections of the NK-1 receptor antagonist SR-140333 before exercise attenuated PEH. The antagonist, in a dose (60 pmol) that blocked substance P- and sparedd,l-homocysteic acid-induced depressor responses, significantly attenuated the PEH by 37%, whereas it had no effect on blood pressure during exercise. Vehicle microinjection had no effect. The antagonist also had no effect on heart rate responses during both exercise and the PEH period. The data suggest that a substance P (NK-1) receptor mechanism in the NTS contributes to PEH.

Melatonin attenuates hypertension-related proarrhythmic myocardial maladaptation of connexin-43 and propensity of the heart to lethal arrhythmias

2013 ◽  
Vol 91 (8) ◽  
pp. 633-639 ◽  
Author(s):  
Tamara Benova ◽  
Csilla Viczenczova ◽  
Jana Radosinska ◽  
Barbara Bacova ◽  
Vladimir Knezl ◽  
...  
Keyword(s):  
Connexin 43 ◽  
Wistar Rats ◽  
Electrical Coupling ◽  
Wistar Rat ◽  
Spontaneously Hypertensive ◽  
Kinase C ◽  
Rat Hearts ◽  
Cx43 Mrna ◽  
Cardioprotective Effects ◽  
Coupling Protein

We hypothesized that the pineal hormone melatonin, which exhibits cardioprotective effects, might affect myocardial expression of cell-to-cell electrical coupling protein connexin-43 (Cx43) and protein kinase C (PKC) signaling, and hence, the propensity of the heart to lethal ventricular fibrillation (VF). Spontaneously hypertensive (SHR) and normotensive Wistar rats fed a standard rat chow received melatonin (40 μg/mL in drinking water during the night) for 5 weeks, and were compared with untreated rats. Melatonin significantly reduced blood pressure and normalized triglycerides in SHR, whereas it decreased body mass and adiposity in Wistar rats. Compared with healthy rats, the threshold to induce sustained VF was significantly lower in SHR (18.3 ± 2.6 compared with 29.2 ± 5 mA; p < 0.05) and increased in melatonin-treated SHR and Wistar rats to 33.0 ± 4 and 32.5 ± 4 mA. Melatonin attenuated abnormal myocardial Cx43 distribution in SHR, and upregulated Cx43 mRNA, total Cx43 protein, and its functional phosphorylated forms in SHR, and to a lesser extent, in Wistar rat hearts. Moreover, melatonin suppressed myocardial proapoptotic PKCδ expression and increased cardioprotective PKCε expression in both SHR and Wistar rats. Our findings indicate that melatonin protects against lethal arrhythmias at least in part via upregulation of myocardial Cx43 and modulation of PKC-related cardioprotective signaling.

Abstract 390: Cardiovascular Effects of the Angiotensin-(1-7) Analogue A1317

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Janaina F Braga ◽  
Neiva Caldeira ◽  
Roberto Q Lautner ◽  
Rodrigo A Fraga-Silva ◽  
Robson A Santos
Keyword(s):  
Arterial Pressure ◽  
Wistar Rats ◽  
Chinese Hamster ◽  
Cardiovascular Effects ◽  
Acute Effect ◽  
No Production ◽  
Acute Administration ◽  
Spontaneously Hypertensive ◽  
Vasorelaxant Effect ◽  
Beneficial Effects

Angiotensin-(1-7) (Ang-(1-7)) has been shown to have anti-hypertensive properties mediated through the receptor Mas . The beneficial effects of the Mas/Ang-(1-7) pathway prompted us to develop Ang-(1-7) analogues and peptides ligands for Mas. In the present study we evaluated the vasorelaxant and anti-hypertensive effect of the analogue A1317. To examine the NO production, chinese hamster ovary (CHO) cells transfected with Mas cDNA were incubated with A1317 at 10 -7 and 10 -6 mol/l for 60 minutes. Subsequently, the slices were mounted for evaluation by confocal microscopy. The vasorelaxant activity of the A1317 was measured in rings from Wistar rats and spontaneously hypertensive rats (SHR) descending thoracic aorta with functional endothelium pre-contracted with phenylephrine (0.1μM). To determine which receptor is involved in the vasorelaxant effect of the peptide experiment was performed in the presence of the Ang-(1-7) antagonist, A-779 (10 μm), in SHR rings. The acute effect of the peptide on arterial pressure was evaluated in male normotensive Wistar rats and SHR. Mean arterial pressure (MAP) and heart rate (HR) were monitored for 5 hours after in bolus administration of different doses of A1317 (0.1-12.5nmol/kg) in conscious animals. A1317 stimulated the NO production in CHO-Mas transfected cells and produced a concentration-dependent vasodilator effect in endothelium-containing aortic rings (Emax=18.97±1.33% in Wistar rings and 38.0±3.3% in SHR rings). The vasorelaxation produced by A1317 was attenuated by A779. Acute administration of A1317 reduced the MAP time and dose-dependently in conscious SHR. The reduction in MAP started to be significant after 130 minutes of the in bolus injection (Δ=-13±2.0mmHg; 0.5nmol/kg). The maximum change in MAP was observed after 4 hours of the in bolus injection (Δ=-21±4.0mmHg; 0.5nmol/kg). A1317 also produced a decrease in MAP of normotensive Wistar rats, however the magnitude of the MAP change was considerably smaller than that observed in SHR (Δ=-8.8±2.0mmHg). There was no significant effect of A1317 on HR of Wistar rats or SHR. These data suggest that the peptide A1317 presents antihypertensive and vasorelaxant properties and may have cardiovascular applications similar to those of Ang-(1-7).

scholarly journals Genetic architecture of Wistar-Kyoto rat and spontaneously hypertensive rat substrains from different sources

2013 ◽  
Vol 45 (13) ◽  
pp. 528-538 ◽  
Author(s):  
Yanli Zhang-James ◽  
Frank A. Middleton ◽  
Stephen V. Faraone
Keyword(s):  
Spontaneously Hypertensive Rat ◽  
Wistar Rat ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat ◽  
Genome Wide ◽  
Daunting Task ◽  
History Of ◽  
Wistar Kyoto ◽  
Complex Relationships ◽  
Relationship Of

The spontaneously hypertensive rat (SHR) has been widely used as a model for studies of hypertension and attention deficit/hyperactivity disorder. The inbred Wistar-Kyoto (WKY) rat, derived from the same ancestral outbred Wistar rat as the SHR, are normotensive and have been used as the closest genetic control for the SHR, although the WKY has also been used as a model for depression. Notably, however, substantial behavioral and genetic differences among the WKY substrains, usually from the different vendors and breeders, have been observed. These differences have often been overlooked in prior studies, leading to inconsistent and even contradictory findings. The complicated breeding history of the SHR and WKY rats and the lack of a comprehensive understanding of the genetic background of different commercial substrains make the selection of control rats a daunting task, even for researchers who are mindful of their genetic heterogeneity. In this study, we examined the genetic relationship of 16 commonly used WKY and SHR rat substrains using genome-wide SNP genotyping data. Our results confirmed a large genetic divergence and complex relationships among the SHR and WKY substrains. This understanding, although incomplete without the genome sequence, provides useful guidance in selecting substrains and helps to interpret previous reports when the source of the animals was known. Moreover, we found two closely related, yet distinct WKY substrains that may provide novel opportunities in modeling psychiatric disorders.

scholarly journals PACAP causes PAC1/VPAC2 receptor mediated hypertension and sympathoexcitation in normal and hypertensive rats

2012 ◽  
Vol 303 (7) ◽  
pp. H910-H917 ◽  
Author(s):  
M. M. J. Farnham ◽  
M. S. Y. Lung ◽  
V. J. Tallapragada ◽  
P. M. Pilowsky
Keyword(s):  
Stress Responses ◽  
Sympathetic Activity ◽  
Spontaneously Hypertensive Rat ◽  
Cardiovascular Effects ◽  
Inhibitory Effect ◽  
Cardiovascular Control ◽  
Ventrolateral Medulla ◽  
Spontaneously Hypertensive ◽  
Vasoactive Intestinal Peptide Receptor

Pituitary adenylate cyclase-activating polypeptide (PACAP) is an excitatory neuropeptide that plays an important role in hypertension and stress responses. PACAP acts at three G protein-coupled receptors [PACAP type 1 receptor (PAC1) and vasoactive intestinal peptide receptor types 1 and 2 (VPAC1 and VPAC2)] and is localized to sites involved in cardiovascular control, most significantly the rostral ventrolateral medulla (RVLM). The RVLM is crucial for the tonic and reflex control of efferent sympathetic activity. Increases in sympathetic activity are observed in most types of hypertension and heart failure. PACAP delivered intrathecally also causes massive sympathoexcitation. We aimed to determine the presence and abundance of the three PACAP receptors in the RVLM, the role, in vivo, of PACAP in the RVLM on tonic and reflex cardiovascular control, and the contribution of PACAP to hypertension in the spontaneously hypertensive rat (SHR). Data were obtained using quantitative PCR and microinjection of PACAP and its antagonist, PACAP(6–38), into the RVLM of anesthetized artificially ventilated normotensive rats or SHRs. All three receptors were present in the RVLM. PACAP microinjection into the RVLM caused sustained sympathoexcitation and tachycardia with a transient hypertension but did not affect homeostatic reflexes. The responses were partially mediated through PAC1/VPAC2 receptors since the effect of PACAP was attenuated (∼50%) by PACAP(6–38). PACAP was not tonically active in the RVLM in this preparation because PACAP(6–38) on its own had no inhibitory effect. PACAP has long-lasting cardiovascular effects, but altered PACAP signaling within the RVLM is not a cause of hypertension in the SHR.

Release of prostaglandins by the mesenteric artery of the renovascular and spontaneously hypertensive rat

1984 ◽  
Vol 62 (1) ◽  
pp. 89-93 ◽  
Author(s):  
Suzanne Desjardins-Giasson ◽  
Jolanta Gutkowska ◽  
Raul Garcia ◽  
Jacques Genest
Keyword(s):  
Wistar Rats ◽  
Spontaneously Hypertensive Rat ◽  
Pressor Response ◽  
Mesenteric Arteries ◽  
Control Group ◽  
Prostaglandin E ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Specific Increase ◽  
Wistar Kyoto

The release of prostaglandin E2 (PGE2) and 6-ketoprostaglandin F1α (6-keto-PGF1α), the stable metabolite of prostacyclin (PGI2), by the perfused mesenteric arteries of renal and spontaneously hypertensive rats (SHR) have been measured. Unstimulated mesenteric arteries from two-kidney one-clip hypertensive rats (2K-1C) released 1.6 times as much PGE2 and 2.7 times as much 6-keto-PGF1α as those of control rats. The release of PGE2 by mesenteric arteries from one-kidney one-clip hypertensive rats (1K-1C) was not significantly different from that of uninephrectomized normotensive rats, but the release of 6-keto-PGF1α was 3.5 times higher in the former than in the latter. Norepinephrine (NE) induced a dose-related increase in perfusion pressure, in PGE2, and 6-keto-PGF1α release in all four groups. However, its effect on the release of PGE2 was more pronounced in 2K-1C than in sham-operated rats. There was no difference between 1K-1C and the uninephrectomized group. The effect of NE on the release of 6-keto-PGF1α was significantly higher for both renal hypertensive groups. These results indicate that the release of PGE2 is more dependent on the loss of renal mass than on hypertension, while the reverse applies to the release of 6-keto-PGF1α. Unstimulated mesenteric arteries from SHR released less PGE2 and less 6-keto-PGF1α than those of Wistar–Kyoto normotensive rats (WKY), but the release was not significantly different from Wistar rats. Under NE stimulation, WKY mesenteric arteries showed almost no increase in release of PGs. Compared with those of Wistar rats, SHR mesenteric arteries showed a greater pressor response to NE, a lower PGE2 release, and the same release of 6-keto-PGF1α. These findings reveal the difficulty of selecting an appropriate control group in studies involving SHR. We concluded that in renal hypertensive rats the specific increase of PGI2 release by arterial tissue may represent an important adaptive mechanism to the elevated blood pressure. However, this mechanism seems not to be involved in SHR.

The Role of the Baroreceptor Reflex in the Cardiovascular Effects of Propranolol in the Conscious Spontaneously Hypertensive Rat

1979 ◽  
Vol 56 (2) ◽  
pp. 163-167 ◽  
Author(s):  
H. A. J. Struyker-Boudier ◽  
J. F. Smits ◽  
H. Van Essen
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Spontaneously Hypertensive Rat ◽  
Cardiovascular Effects ◽  
Hypotensive Effect ◽  
Baroreceptor Reflex ◽  
Acute Effects ◽  
Spontaneously Hypertensive

1. The role of baroreceptors in the cardiovascular mechanism of action of dl-propranolol has been studied by comparing the acute effects of subcutaneous injection of 1 and 5 mg/kg (3·3 × 10−6 and 16·5 × 10−6 mol/kg) of this drug in conscious baroreceptor-denervated spontaneously hypertensive (SH) rats with those in sham-operated control SH rats. 2. At 5 mg/kg (16·5 × 10−6 mol/kg) propranolol caused a small, but significant, increase in blood pressure in sham-operated SH rats, whereas both after 1 and 5 mg/kg (3·3 × 10−6 and 16·5 × 10−6 mol/kg) immediate hypotension was observed in baroreceptor-denervated animals. 3. Heart rate dropped rapidly after injection of 1 or 5 mg/kg (3·3 × 10−6 and 16·5 × 10−6 mol/kg) propranolol both in the baroreceptor-denervated and sham-operated SH rats. Bradycardia was significantly larger in the baroreceptor-denervated animals after an injection of 5 mg/kg (16·5 × 10−6 mol/kg). 4. It is concluded that the lack of an early hypotensive effect of propranolol in intact animals is caused by an increased baroreceptor reflex activity as a consequence of the fall in cardiac output.

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