Evidence for contribution of effector organ cellular responses to the biphasic dynamics of heat acclimation

Abstract

The involvement of cellular processes in the biphasic dynamics of heat acclimation was studied. Key steps in the cholinergic signal transduction pathway for water secretion were measured in the submaxillary gland of acclimating [2-day short-term heat acclimation (STHA) and 30-day long-term heat acclimation (LTHA) at 34 degrees C] or acute heat-stressed (2 h at 40 degrees C) rats in vitro. Both the carbamylcholine (CCh)-induced maximal fractional rate and the total 86Rb+ efflux, reflecting K+ efflux and water transport, transiently decreased in STHA (P < 0.001). In LTHA, the total K+ efflux increased (P < 0.001), whereas the maximal fractional rate of efflux increased only slightly. During STHA, the density of the high-affinity binding site of the muscarinic receptors (MRs) increased by 50% and their affinity for the muscarinic antagonist [3H]-N-methylscopolamine decreased transiently by 87%. Basal cytosolic Ca2+ concentration ([Ca2+]i) decreased (P < 0.05), but the peak CCh-induced [Ca2+]i increase resembled the control values. In LTHA, MR density continued to increase (100%; P < 0.05), whereas affinity resumed control values. Basal and CCh-induced [Ca2+]i increases returned to control levels. We conclude that glandular cellular processes follow a biphasic pattern with major apparent changes attributable to events distal to the [Ca2+]i rise. This was further validated by employing heat stress, which produced qualitatively different effects on the MR profile with a decrease in 86Rb+ efflux comparable to STHA. Hence, although heat-induced changes in the proximal components of the signal transduction pathway may contribute to altered regulatory span, the predominant apparent cellular effect is on the distal part of the pathway.

Metabolic and hormonal acclimation to heat stress in domesticated ruminants

“…There is evidence for a temporal biphasic pattern of heat acclimation: short-term and long-term heat acclimations (STHA and LTHA, respectively;Horowitz et al, 1996;Hahn, 1999;Horowitz, 2002). STHA is the phase in which changes are initiated within cellular signalling pathways (Horowitz et al, 1996) leading to disturbances in cellular homeostasis and begins to reprogram cells to survive the deleterious effects of heat stress (Horowitz, 2001).…”

“…In addition, acclimatory responses possess a hormonal link in the pathway from the central nervous system to the effector cells, and usually alter the response of effector cells or organs to an environmental challenge. The main effect of these acclimatory responses is to coordinate metabolism to achieve a new equilibrium that could be considered as a new physiological state.There is evidence for a temporal biphasic pattern of heat acclimation: short-term and long-term heat acclimations (STHA and LTHA, respectively;Horowitz et al, 1996;Hahn, 1999;Horowitz, 2002). STHA is the phase in which changes are initiated within cellular signalling pathways (Horowitz et al, 1996) leading to disturbances in cellular homeostasis and begins to reprogram cells to survive the deleterious effects of heat stress (Horowitz, 2001).…”

“…STHA is the phase in which changes are initiated within cellular signalling pathways (Horowitz et al, 1996) leading to disturbances in cellular homeostasis and begins to reprogram cells to survive the deleterious effects of heat stress (Horowitz, 2001). In rodents, the full expression of STHA is attained when the drop in plasma thyroid hormones (T3 and T4) level exceeds 30% to 40% (Horowitz, 2001).…”

Ethnic differences in thermoregulation: Genotypic versus phenotypic heat adaptation

“…Instead, it is hypothesised that the appearance of a lower sweat rate in such indigenes is an example of thermoregulatory habituation (negative phenotypic adaptation), and is indicative of a superior overall heat adaptation, possibly representing an extension of the two adaptation stages identified by Horowitz et al (1996). In fact, a large number of investigators have reported lower sweat responses in indigenous people from several continents, in comparison with Caucasians exposed to an equivalent heat stress: Thompson (1954: Negroid); Edholm et al (1964: Indians); McCance and Purohit (1969: Indians and Negroid); Fox et al (1974: New Guineans) McCance et al (1974: Bedouin); Samueloff (1987: Indians); Duncan and Horvath (1988: tropical Asians).…”

Cutaneous thermal thresholds of tropical indigenes residing in Japan

“…It is known that heat adaptation is manifested at various levels throughout the body; i.e. the subcellular, cellular, organ, and systemic levels (Adam et al, 1960;Horowitz et al, 1996). It has been proposed that changes in cutaneous thermal sensitivity are induced by alterations in the structure and function of cutaneous thermal receptors (Brück, 1986), such as decreases in the number or size of warm/cold spots in the skin or changes in the neurotransmission speed of nerves (Meliala et al, 1999) and a reduced maximum firing activity of single cold responsive units (Hinckel and Schroder-Rosenstock, 1982).…”