It has recently been demonstrated in week‐old rats that extreme cold challenges that lead to significant bodily cooling result in decreased cardiac rate. To determine whether pups are able to maintain arterial pressure in the face of decreasing cardiac rate in extreme cold, we measured blood pressure in unanesthetized week‐old rats. Instrumented pups were thermally challenged and thermoregulatory and cardiovascular responses were monitored. Despite pronounced decreases in cardiac rate in the cold, pups were able to maintain mean arterial pressure (MAP), presumably by increasing peripheral resistance. At the lowest air temperature (17°C) pups emitted ultrasonic vocalizations, and these emissions were accompanied by pulsatile increases in intraabdominal pressure (IAP) and MAP. We hypothesize that these pulsatile increases in IAP during extreme cooling reflect the use of the abdominal compression reaction to increase venous return during periods of diminished cardiac output. © 1998 John Wiley & Sons, Inc. Dev Psychobiol 32: 169–176, 1998

Infants rats depend on heat production by brown adipose tissue (BAT) during cold challenge. Although it has been suggested that BAT thermogenesis protects the heart in the cold, the relationship of BAT activation to cardiac rate has not been examined directly. In the first experiment, the cardiac rate of 2- and 7- to 8-day-old rat pups was monitored during moderate and extreme cold challenge. Pups at both ages maintained cardiac rate during moderate cold challenge while BAT thermogenesis was increasing. In contrast, cooling to air temperatures at which BAT thermogenesis could increase no further resulted in pronounced bradycardia. In the second experiment, ganglionic blockade was used to eliminate BAT heat production and autonomic control of the heart in 7- to 8-day olds. Blockade suppressed BAT thermogenesis in the cold and led to pronounced decreases in interscapular temperature and cardiac rate. These data suggest that cardiac rate in infant rats is modulated both by the autonomic nervous system and BAT thermogenesis.

Concerns have been raised frequently about caffeine's potential for increasing blood pressure (BP) and posing a risk for cardiovascular disease. This review surveys research concerning the effects of caffeine on BP and heart rate (HR). Tolerance to caffeine, family history of hypertension, borderline hypertension, and hypertension are also examined as potential moderators. Results from epidemiological studies are inconsistent. Experimental laboratory studies have generally found that caffeine produces acute rises in systolic and diastolic BP that are additive to any stress-induced increases. Synergistic effects which might pose a more serious risk are rarely found. Heart rate data are less consistent, possibly due to the different ways HR is measured. Tolerance to the cardiovascular effects of caffeine has reliably been reported; however, overnight abstinence may be sufficient to negate tolerance effects to most levels of caffeine ingestion in typical caffeine users. Though caffeine drinkers may exhibit acute increases in BP, the long-term effects appear to be minimal. However, persons at risk for hypertension may be more vulnerable to the BP effects of caffeine.

Ultrasonic vocalizations emitted by infant rodents are typically characterized as cries of distress. There are two contexts that are known to reliably elicit ultrasound production: extreme cold exposure and administration of clonidine, an alpha 2 adrenoceptor agonist. Noting that these two contexts both entail pronounced decreases in cardiac rate, we have hypothesized that the vocalizations are acoustic by-products of a physiological maneuver, the abdominal compression reaction (ACR), that increases venous return to the heart when return is compromised. As a critical test of this hypothesis, we measured venous pressure near the right atrium in 15-day-old rats after clonidine administration. Consistent with the ACR hypothesis, emission of ultrasound was accompanied by large and reliable increases in venous pressure and, therefore, venous return. These results provide strong, direct support for the ACR hypothesis and, by doing so, underscore the potential pitfalls of anthropomorphic interpretations of the vocalizations of infant rats.

The role of central nervous system arginine vasopressin (AVP) and oxytocin (OXY) in the cardiovascular response to acute stress was examined using three experimental models: pharmacological antagonism of central AVP-OXY receptors; lesions of the paraventricular nucleus (PVN); and rats genetically lacking in AVP synthesis, i.e., the Brattleboro strain. Central administration of an AVP-OXY antagonist abolished the increase in heart rate (HR) seen following acute footshock stress. The group receiving centrally administered antagonist increased HR 15 +/- 17 (SE) beats/min, whereas, in contrast, the group receiving intravenous administration of the antagonist showed a 66 +/- 17 beats/min increase, and the group receiving intraventricular antagonist vehicle showed a 101 +/- 14 beats/min increase in response to stress. In a second study, electrolytic lesions of the PVN also blocked the increase in HR seen following stress, 20 +/- 12 beats/min for PVN-lesioned rats, 74 +/- 25 beats/min for sham lesion rats, and 93 +/- 7 beats/min for rats with a lesion not destroying the PVN. In the final study, the responses of Brattleboro rats, i.e., rats genetically deficient in vasopressin synthesis, were equivalent to their Long-Evans controls (131 +/- 13 and 147 +/- 12 beats/min, respectively). In each of these studies, the blood pressure responses to the stressor were equivalent for control and experimental groups. The results of these studies suggest that a neuropeptide system originating in or passing through the PVN may play an important role in the cardiovascular responses to stress and further suggest that the central OXY system may be one pathway mediating this response.