Effects of natriuretic peptides on vascular smooth-muscle cells derived from different vascular beds.

1. This study explored the hypothesis that atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-natriuretic peptide (CNP) have differing antiproliferative and antihypertrophic effects on pulmonary artery (PA) and thoracic aorta (TA) smooth-muscle cells (SMCs). 2. Cultured cells were exposed to 5% fetal calf serum (FCS) and angiotensin II (A-II) to induce DNA and protein synthesis, respectively. 3. ANP (10(-7) M) significantly reduced thymidine uptake in TA by 31% +/- 2% (P < or = 0.01) but not in PA (P > or = 0.05). 4. In parallel experiments, BNP (10(-7) M) significantly reduced thymidine uptake in TA (-22% +/- 5%, P < or = 0.01), but not in PA cells (P > or = 0.05). 5. CNP (10(-7) M) did not significantly alter thymidine uptake in TA cells exposed to FCS, but it did significantly reduce uptake in PA (-28.5% +/- 4%) 2(P < or = 0.05). 6. Blunting by ANP (10(-7) M) of the A-II (10(-8) M)-induced increase in protein synthesis was significantly greater in PA than in TA cells. 7. However, BNP and CNP (10(-7) M) exerted similar antihypertrophic effects on TA and PA cells exposed to A-II. 8. The antiproliferative effects of BNP and ANP exceed those of CNP in TA SMCs, but CNP appears to be the most effective antiproliferative agent in PA SMCs. In addition, PA-derived SMCs are more sensitive to the antihypertrophic effects of ANP than TA-derived cells, suggesting phenotypic differences. The findings indicate that the natriuretic peptides may play complementary roles in modulating SMC proliferation and protein synthesis.

Neonatally-induced thermotolerance: physiological responses.

1. Broiler cockerels exposed to neonatal heat (35-37.8 degrees C for 24 hr) at 5 days of age experienced significantly lower mortality upon exposure to elevated temperatures (35-37.8 degrees C) at 43 days of age than did cockerels not given neonatal heat exposure. 2. No differences were found between neonatally stressed and neonatal control groups in water consumption, core and surface temperature, plasma T3 and T4, protein or glucose concentration when exposed to juvenile heat stress. 3. Heterophil to lymphocyte ratios were significantly lower in the neonatally stressed than in the neonatal control group when exposed to heat at 44 days of age. 4. The results indicate that lower mortality during periods of high environmental temperature in the neonatally stressed chicks may involve homeostatic mechanisms different from those utilized during acclimation to high environmental temperature.

Effect of heat stress early in life on mortality of broilers exposed to high environmental temperatures just prior to marketing.

A study was conducted to investigate the effects of heat stress during the 1st wk of life on subsequent mortality resulting from exposure to high environmental temperature and feed restriction just prior to marketing of broiler cockerels. Birds were raised under standard husbandry procedures except that at 5 days of age, half the broilers were heat stressed by exposure to an environmental temperature ranging from 35.0 to 37.8 C for 24 h while the remaining birds were held at 29.4 C. At 44 and 45 days of age, half the unstressed controls and half the birds stressed at 5 days of age were exposed to temperatures ranging from 35.0 to 37.8 C for 8 h/day. In a factorial arrangement of treatments, the effect of restricting feed for 8 h/day on Days 43, 44, and 45 was also examined. Exposing birds to high environmental temperatures at 5 days of age resulted in a significant decrease in mortality when birds were exposed to a high environmental temperature later in life. In addition, feed efficiency was improved significantly in early heat-stressed birds whereas body weight and body weight gain were not affected. Feed restriction had no significant effect on mortality, body weight, or feed efficiency. It appears, therefore, that exposing broiler cockerels to mild heat stress for 24 h at 5 days of age can significantly decrease mortality resulting from high environmental temperature later in life.