Sex differences and the role of ovarian hormones in site-specific nociception of SHR

Accurate diagnosis and treatment of pain is dependent on knowledge of the variables that might alter this response. Some of these variables are the locality of the noxious stimulus, the sex of the individual, and the presence of chronic diseases. Among these chronic diseases, hypertension is considered a serious and silent disease that has been associated with hypoalgesia. The main goal of this study was to evaluate the potential nociceptive differences in spontaneously hypertensive rats (SHR) regarding the locality of the stimulus, i.e., the temporomandibular joint or paw, the sex, and the role of ovarian hormones in a model of mechanical nociception (Von Frey test) or formalin-induced inflammatory nociception. Our results indicate that SHR had lower orofacial mechanical nociception beyond the lower mechanical nociception in the paw compared with WKY rats. In a model of formalin-induced inflammatory nociception, SHR also had decreased nociception compared with normotensive rats. We also sought to evaluate the influence of sex and ovarian hormones on orofacial mechanical nociception in SHR. We observed that female SHR had higher mechanical nociception than male SHR only in the paw, but it had higher formalin-induced orofacial nociception than male SHR. Moreover, the absence of ovarian hormones caused an increase in mean arterial pressure and a decrease in paw nociception in female SHR.

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Estrogen depletion induces NaCl-sensitive hypertension in female spontaneously hypertensive rats

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.2001.281.6.r1934 ◽

2001 ◽

Vol 281 (6) ◽

pp. R1934-R1939 ◽

Cited By ~ 41

Author(s):

Zhiwu Fang ◽

Scott H. Carlson ◽

Y. F. Chen ◽

S. Oparil ◽

J. Michael Wyss

Keyword(s):

Nervous System ◽

Arterial Pressure ◽

Spontaneously Hypertensive Rats ◽

Physiological Role ◽

Ovarian Hormones ◽

Hypertensive Rats ◽

Spontaneously Hypertensive ◽

Sympathetic Nervous ◽

Estrogen Depletion

In women, arterial pressure generally increases after menopause, but several studies suggest that women who eat large amounts of plant estrogens (phytoestrogens) experience a slower rise in the incidence of postmenopausal hypertension. This suggests that both ovarian hormones (principally estrogen) and phytoestrogens may protect at least some women from hypertension. The present study tests the hypothesis that phytoestrogens blunt hypertension in estrogen-depleted female spontaneously hypertensive rats (SHR). Three-week-old ovariectomized SHR were fed one of four diets that contained basal (0.6%) or high (8%) NaCl with or without dietary phytoestrogens for 9 wk. In SHR on the basal NaCl diet, arterial pressure was unaffected by the removal of dietary phytoestrogens. In contrast, in SHR on the high-NaCl diet, arterial pressure was significantly higher in rats on the phytoestrogen-free (204 ± 4 mmHg) compared with the phytoestrogen-replete (153 ± 4 mmHg) diet. Ganglionic blockade resulted in reductions in arterial pressure that were directly related to the dietary NaCl-induced increases in arterial pressure. Together, these data indicate that dietary phytoestrogens protect ovariectomized female SHR from dietary NaCl-sensitive hypertension and that the sympathetic nervous system plays an important role in this effect. Furthermore, these results demonstrate that dietary phytoestrogens can have a major impact on the interpretation of studies into the physiological role of estrogen in females.

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THE ROLE OF CALCIUM-PROTEIN KINASE C SYSTEMS IN THE REGULATION OF ACETYLCHOLINE RELEASE IN THE CENTRAL NERVOUS SYSTEM OF SPONTANEOUSLY HYPERTENSIVE RATS

Japanese Heart Journal ◽

10.1536/ihj.37.532 ◽

1996 ◽

Vol 37 (4) ◽

pp. 532-532

Author(s):

Kazushi Tsuda ◽

Ichiro Nishio ◽

Yoshiaki Masuyama

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Protein Kinase C ◽

Spontaneously Hypertensive Rats ◽

Acetylcholine Release ◽

Hypertensive Rats ◽

Spontaneously Hypertensive ◽

Kinase C ◽

The Central Nervous System

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Role of nuclear proto-oncogenes in the proliferation of aortic smooth muscle cells in spontaneously hypertensive rats

Journal of Hypertension ◽

10.1097/00004872-198900076-00053 ◽

1989 ◽

Vol 7 ◽

pp. S114-115 ◽

Cited By ~ 7

Author(s):

Maryvonne Baudouin-Legros ◽

Jean-Luc Paquet ◽

Gilles Brunelle ◽

Philippe Meyer

Keyword(s):

Smooth Muscle ◽

Smooth Muscle Cells ◽

Spontaneously Hypertensive Rats ◽

Muscle Cells ◽

Hypertensive Rats ◽

Spontaneously Hypertensive ◽

Aortic Smooth Muscle Cells ◽

Aortic Smooth Muscle

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Increased Pressor Responsiveness to Enkephalin in Spontaneously Hypertensive Rats: The Role of Vasopressin

Clinical Science ◽

10.1042/cs059235s ◽

1980 ◽

Vol 59 (s6) ◽

pp. 235s-237s ◽

Cited By ~ 17

Author(s):

R. W. Rockhold ◽

J. T. Crofton ◽

L. Share

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Pressor Response ◽

Cardiovascular Effects ◽

Hypertensive Rats ◽

Methionine Enkephalin ◽

Spontaneously Hypertensive ◽

Wistar Kyoto Rats ◽

Wistar Kyoto

1. The cardiovascular effects of an enkephalin analogue were examined in spontaneously hypertensive and normotensive Wistar-Kyoto rats. (D-Ala2)-methionine enkephalin caused a biphasic increase in blood pressure and an increase in heart rate after intracerebroventricular injection. 2. The initial pressor response to (D-Ala2)-methionine enkephalin was greater in hypertensive than in normotensive rats. No difference was noted between groups during the secondary pressor response. Heart rate increases paralleled the secondary increase in blood pressure. 3. Naloxone pretreatment abolished the secondary increase in blood pressure and the tachycardia, but did not blunt the initial pressor response in female Wistar-Kyoto rats. 4. Plasma levels of arginine vasopressin were depressed during the plateau phase of the pressor response in hypertensive rats given intracerebroventricular (d-Ala2)-methionine enkephalin. 5. The results suggest that the cardiovascular effects of central enkephalin are not due to vasopressin, but may involve activation of the sympathetic nervous system.

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