Cold-induced Hypertension Research Articles

Role of the sympathetic nervous system in cold-induced hypertension in rats

Hypertension develops in rats exposed chronically to cold [6 +/- 2 degrees C (SE)] and includes both an elevation of mean arterial pressure and cardiac hypertrophy. Previous studies suggest that cold-exposed animals, at least initially, have a large sustained increase in the activity of their sympathetic nervous system, suggesting a failure of the baroreceptor system to provide sufficient negative feedback to the central nervous system. The present study was designed to investigate whether alterations in the activity of the sympathetic nervous system, including the baroreceptor reflex, occur during exposure to cold and whether they contribute to cold-induced hypertension. Twenty male rats were prepared with indwelling catheters in the femoral artery and vein. Ten of the rats were exposed to cold (6 +/- 2 degrees C) chronically, while the remaining 10 were kept at 26 +/- 2 degrees C. Withdrawal of arterial blood samples (less than 5 ml/kg), measurement of direct arterial pressures, and measurement of baroreflex function were carried out at 0800 h at intervals throughout the experiment. Norepinephrine and epinephrine concentrations in plasma were also determined at intervals throughout the experiment. Systolic, diastolic, and mean blood pressures of cold-exposed rats were increased to levels significantly above those of controls. The sensitivity of the baroreflex (delta heart period/delta mean arterial pressure) was decreased in the cold-treated group. The concentration of norepinephrine in plasma increased after 24 h of exposure to cold and remained elevated throughout the experiment, whereas the concentration of epinephrine in plasma increased initially but returned to control levels after 19 days of exposure to cold.(ABSTRACT TRUNCATED AT 250 WORDS)

Prevention of cold-induced increase in blood pressure of rats by captopril.

To assess the possibility that the renin-angiotensin system may play a role in the development of cold-induced hypertension, three groups of rats were used. Two groups were exposed to cold (5 +/- 2 degrees C) while the remaining group was kept at 26 +/- 2 degrees C. One group of cold-treated rats received food into which captopril (0.06% by weight) had been thoroughly mixed. The remaining two groups received the same food but without captopril. Systolic blood pressure of the untreated, cold-exposed group increased significantly above that of the warm-adapted, control group within 4 weeks of exposure to cold. In contrast, chronic treatment with captopril prevented the elevation of blood pressure. Rats were killed after 4 months of exposure to cold. At death, the heart, kidneys, adrenal glands, and interscapular brown fat pad were removed and weighed. Although captopril prevented the elevation of blood pressure in cold-treated rats, it did not prevent hypertrophy of the kidneys, heart, and interstitial brown adipose tissue that characteristically accompanies exposure to cold. Thus, chronic treatment with captopril prevented the elevation of blood pressure when administered at the time exposure to cold was initiated. It also reduced the elevated blood pressure of cold-treated rats when administered after blood pressure became elevated. This suggests that the renin-angiotensin system may play a role in the elevation of blood pressure during exposure to cold.

Effect of Chronic Dietary Treatment with Z-Tryptophan on the Development of Cold-Induced Hypertension in Rats

This study was designed to assess the effect of chronic dietary administration (2.5 and 5.0% by weight) of the neutral amino acid, L-tryptophan, on the development of hypertension during chronic exposure to cold. In addition, a warm-adapted and cold-treated control group receiving unsupplemented food were used. Chronic administration of the lower dose of L-tryptophan (850 mg/day) prevented the elevation of blood pressure attenuated cardiac hypertrophy, and had no effect on body weight during exposure to cold. The higher dose of L-tryptophan (1,690 mg/day) attenuated the rate of blood pressure increase, did not affect cardiac hypertrophy, attenuated the gain in body weight, and increased the urinary output of epinephrine. Thus, this dose may be associated with some toxicity. Both doses of tryptophan failed to prevent certain other responses characteristically occurring during exposure to cold: i.e. increased weight of the kidneys, adrenal glands and brown adipose tissue; increased food and water consumption; increased dipsogenic responsiveness to angiotensin II, and increased plasma aldosterone concentration. The results indicate that chronic dietary administration of L-tryptophan (850 mg/day) can prevent the development of cold-induced hypertension, as it can in all other models of hypertension tested thus far in rats.

Factors Affecting Cold-Induced Hypertension in Rats

A 3- to 4-week exposure of rats to a cold environment (5 +/- 2 degrees C) induces hypertension, including elevation of systolic, diastolic, and mean blood pressures and cardiac (left ventricular) hypertrophy. The studies described here were designed to investigate some factors affecting both the magnitude and the time course for development of cold-induced hypertension. The objective of the first study was to determine whether there was an ambient temperature at which the cold-induced elevation of blood pressure did not occur. The objective of the second experiment was to determine whether body weight at the time of exposure to cold affected the magnitude and time course for development of hypertension. To assess the first objective, male rats were housed in a chamber whose temperature was maintained at 5 +/- 2 degrees C while others were housed in an identical chamber at 9 +/- 2 degrees C. After 7 days of exposure to cold, the rats exposed to the colder temperature had a significant elevation of blood pressure (140 +/- 2 mm Hg) compared with the group maintained at 9 degrees C (122 +/- 3 mm Hg). The rats exposed to 9 degrees C had no significant elevation of systolic blood pressure at either 27 or 40 days after initiation of exposure to cold. At the latter time, the temperature in the second chamber was reduced to 5 +/- 2 degrees C. By the 25th day of exposure to this ambient temperature, the rats had a significant increase in systolic blood pressure above their levels at 9 degrees C. Thus, there appears to be a threshold ambient temperature for elevation of blood pressure during exposure to cold. That temperature appears to lie somewhere between 5 and 9 degrees C. The second objective was assessed by placing rats varying in weight from approximately 250 to 430 g in air at 5 degrees C. There was a highly significant direct relationship (r = 0.96) between body weight at the time of introduction to cold and the number of days required to increase systolic blood pressure by 10 mm Hg above pre-cold exposure level. The third objective was to make an initial assessment of potential differences among strains of rats with respect to development of cold-induced hypertension. To this end, rats of the Fischer 344 strain were used. Systolic blood pressures of these rats also increased during chronic exposure to cold.(ABSTRACT TRUNCATED AT 400 WORDS)

Reversibility of cold-induced hypertension after removal of rats from cold

Chronic exposure of rats to cold air induces hypertension, including elevation of blood pressure and cardiac hypertrophy. The present study was designed to assess reversibility of these changes after removal from cold. Five groups of six male rats each were exposed to cold (5 +/- 2 degrees C) for 39 days, while six control rats were maintained at 26 +/- 2 degrees C. Systolic blood pressures of the rats in one of the cold-treated groups, as well as the controls, were measured twice weekly throughout the experiment. Blood pressure of the cold-exposed rats (150 +/- 3 mmHg; 1 mmHg = 133.3 Pa) became elevated significantly above that of controls (129 +/- 3 mmHg) within 4 weeks. On day 39 of cold exposure, one group (six rats) of the cold-treated rats was sacrificed while still in the cold. The remaining four groups of cold-treated rats were than removed from cold and kept at 26 +/- 2 degrees C. One group of cold-treated rats was sacrificed weekly thereafter. During the last week, the six control rats were also sacrificed. At death, the heart, kidneys, and adrenal glands were removed and weighed. Mean heart weight of the cold-treated group (346 +/- 7 mg/100 g body weight), sacrificed prior to removal from cold, was significantly (p less than 0.01) greater than that of controls (268 +/- 5 mg/100 g body weight). The increased heart weight of the cold-treated group appeared to result mainly from an increase in left ventricular weight.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of extremes of temperature on hypertensive rats.

ArticleEffects of Extremes of Temperature on Hypertensive RatsMelvin J. FreglyMelvin J. FreglyFrom the Department of Physiology, Harvard Medical School, Boston, MassachusettsPublished Online:31 Jan 1954https://doi.org/10.1152/ajplegacy.1954.176.2.275MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByIntermittent cold exposure improves glucose homeostasis despite exacerbating diet‐induced obesity in mice housed at thermoneutrality12 July 2021 | The Journal of Physiology, Vol. 600, No. 4Animal models for the study of primary and secondary hypertension in humans18 October 2016 | Biomedical Reports, Vol. 5, No. 6Experimental animal models of hypertensionJournal of the American Society of Hypertension, Vol. 3, No. 3Opposite regulation of brain angiotensin type 1 and type 2 receptors in cold-induced hypertensionRegulatory Peptides, Vol. 97, No. 2-3Reduction of Cold-Induced Hypertension by Antisense Oligodeoxynucleotides to Angiotensinogen mRNA and AT 1 -Receptor mRNA in Brain and BloodHypertension, Vol. 31, No. 6Melvin J. Fregly.Annals of the New York Academy of Sciences, Vol. 813, No. 1 ThermoregulatAdaptations: Some General Characteristics1 January 2011Effects of cold acclimation and central opioid processes on thermoregulation in ratsPharmacology Biochemistry and Behavior, Vol. 54, No. 2Effect of renal denervation on elevation of blood pressure in cold-exposed ratsCanadian Journal of Physiology and Pharmacology, Vol. 73, No. 1Prevention of cold-induced increase in blood pressure of rats by captopril.Hypertension, Vol. 17, No. 6_pt_1Changes in blood pressure and dipsogenic responsiveness to angiotensin II during chronic exposure of rats to coldPharmacology Biochemistry and Behavior, Vol. 38, No. 4Effects of Environmental Stresses and Privations on ThirstGoldblatt hypertension and operant thermoregulation in shaved, sialoadenectomized ratsPhysiology & Behavior, Vol. 45, No. 4Influence of the Pineal Gland and Melatonin on Blood Flow and Evaporative Water Loss During Heat Stress in RatsJournal of Pineal Research, Vol. 4, No. 2Water and electrolyte exchange during exposure to coldPharmacology & Therapeutics, Vol. 18, No. 2Regulation of sodium chloride intake by normotensive and hypertensive rats∗The American Journal of Cardiology, Vol. 8, No. 6Effect of Treatment with Radioactive Iodine and Iodine-Deficient Diet on Development and Maintenance of Renal Hypertension in RatsCirculation Research, Vol. 8, No. 4Physiologic and Anatomic Effects of Propylthiouracil on Normal and Hypertensive RatsCirculation Research, Vol. 7, No. 3 More from this issue > Volume 176Issue 2January 1954Pages 275-281 Copyright & PermissionsCopyright © 1954 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1954.176.2.275PubMed13124531History Received 30 September 1953 Published online 31 January 1954 Published in print 31 January 1954 Metrics