Thermoregulatory and Cardiac Responses of Infant Spontaneously Hypertensive and Wistar-Kyoto Rats to Cold Exposure

Abstract

Abstract-Cardiovascular function during cold exposure is dependent on effective thermoregulation. This dependence is particularly apparent in infants. For example, we have previously demonstrated that in infant rats during cold exposure, cardiac rate is directly related to their ability to produce heat endogenously. The primary source of endogenous heat production for infant rats is brown adipose tissue (BAT). Because of the dependence of cardiac rate on effective thermoregulation in the cold and because hypertension in spontaneously hypertensive rats (SHR) is influenced by the preweanling environment, in this study we examined the thermoregulatory and cardiac rate responses of infant SHR and Wistar-Kyoto rats (WKY) to varying levels of cold exposure. In experiment 1, 7-to 8-day-old SHR and WKY were acclimated at a thermoneutral air temperature (35°C) and then exposed to successive decreases in ambient temperature (30.5°C, 26.5°C, 23°C, and 17°C) while thermal and metabolic measures were recorded. Although both strains increased BAT thermogenesis and oxygen consumption in response to cold exposure, SHR cooled more than WKY and exhibited lower levels of oxygen consumption at the lowest air temperatures. Experiment 2 was identical to experiment 1 except that cardiac rate was also measured. Again, SHR exhibited substantial thermoregulatory deficits compared with WKY; in addition, they were less able than WKY to maintain cardiac rate at the 2 lowest air temperatures tested. Finally, in experiment 3, infant SHR exhibited diminished BAT thermogenesis in response to a range of doses of a selective ␤ 3 -adrenoceptor agonist. We hypothesize that long-term thermoregulatory deficits during the early postnatal period influence cardiovascular function and contribute to the development of hypertension in SHR. (Hypertension. 1999;33:1465-1469.)Key Words: body temperature regulation Ⅲ brown fat Ⅲ nonshivering thermogenesis Ⅲ heart rate Ⅲ rats, inbred strains Ⅲ hypertension, experimental T he degree of high blood pressure expressed in adult spontaneously hypertensive rats (SHR) is influenced by the neonatal environment. 1-3 Thus, manipulations limited to the preweanling period, such as cross-fostering, 2 pharmacological interventions, 1,4 and handling, 5,6 result in the lowering of blood pressure in adult SHR. Such findings highlight the importance of epigenetic processes in the development of established hypertension in SHR.We have recently demonstrated that thermoregulatory mechanisms play an important role in the protection of cardiovascular function during cold exposure in infant rats. [7][8][9] Specifically, heat produced by brown adipose tissue (BAT) during moderate cold exposure helps to warm cardiac muscle and by doing so contributes to the maintenance of cardiac rate. In contrast, pronounced bradycardia is produced by either extreme air temperatures that overwhelm the ability of BAT to deliver warm blood to cardiac muscle or ganglionic blockade that prevents the activation of BAT thermogenesis in response to the cold.T...

Cardiovascular and metabolic responses of hypertensive and normotensive rats to one week of cold exposure

“…T a has sometimes been reported to have different effects on metabolic rate (V O 2 ) in SHRs and normotensive Wistar-Kyoto controls. Strain differences were reported in adult rats when T a was in the range 25-32°C (38) and in infant rats when the T a range was 17-23°C (18). However, others have reported no differences in V O 2 between these strains in cold (5°C) or warm (35°C) conditions (37).…”

Prairie vole pups show potentiated isolation‐induced vocalizations following isolation from their mother, but not their father

“…Communicatory functions of USV, which are almost by definition social, have been repeatedly demonstrated: calls by pups guide and elicit retrieval by their mothers (Bowers, Perez‐Pouchoulen, Edwards, & McCarthy, ; Brunelli, Shair, & Hofer, ; Ehret, ; Sewell, ). Although there have been attempts to attribute USV production to thermoregulatory (Blumberg & Alberts, ; Blumberg, Efimova, & Alberts, ; Blumberg & Sokoloff, ) and/or cardiovascular processes (Blumberg, Sokoloff, & Kent, ; Kirby & Blumberg, ; Kirby, Sokoloff, Perdomo, & Blumberg, ), these hypotheses have not been supported by direct tests (Hofer & Shair, ; Shair, Brunelli, Masmela, Boone, & Hofer, ; Shair & Jasper, ), and summarized in (Shair, ), except in the case of recovery from deep hypothermia (Hofer & Shair, ).…”

Inherited stress-induced hypertension associates with altered gene expression of thermosensitive TRP ion channels in hypothalamus

“…Temperature is an important environmental factor and no wonder that it occupies the first line in the table summarizing the factors affecting the blood pressure [4]. It should be emphasized that the elevated blood pressure in the warm-blooded organisms has pronounced effects on their responses to the temperature changes [5][6][7][8][9]. The study of the physiological responses to the cooling test in rats with inherited stress-induced arterial hypertension (the ISIAH rat strain) demonstrated considerable differences between hypertensive and normotensive animals in thermoregulatory responses, both vasoconstrictor and metabolic, and in the threshold temperatures of the thermoregulatory responses [10].…”