Histological modifications of the rat prostate following transection of somatic and autonomic nerves

It is known that hormones influence significantly the prostate tissue. However, we reported that mating induces an increase in androgen receptors, revealing a neural influence on the gland. These data suggested that somatic afferents (scrotal and genitofemoral nerves) and autonomic efferents (pelvic and hypogastric nerves) could regulate the structure of the prostate. Here we assessed the role of these nerves in maintaining the histology of the gland. Hence, afferent or efferent nerves of male rats were transected. Then, the ventral and dorsolateral regions of the prostate were processed for histology. Results showed that afferent transection affects prostate histology. The alveoli area decreased and increased in the ventral and dorsolateral prostate, respectively. The epithelial cell height increased in both regions. Efferent denervation produced dramatic changes in the prostate gland. The tissue lost its configuration, and the epithelium became scattered and almost vanished. Thus, afferent nerves are responsible for spinal processes pertaining to the trophic control of the prostate, activating its autonomic innervation. Hence, our data imply that innervation seems to be synergic with hormones for the healthy maintenance of the prostate. Thus, it is suggested that some prostate pathologies could be due to the failure of the autonomic neural pathways regulating the gland.

Sabe-se que os hormônios influenciam significativamente o tecido prostático. Entretanto, nós demonstramos que o acasalamento induz um aumento nos receptores androgênicos, revelando uma influência neural sobre a glândula. Esses dados sugerem que os aferentes somáticos (nervos escrotal e genito-femural) e os eferentes autonômicos (nervos pélvicos e hipo-gástricos) poderiam regular a estrutura da próstata. Neste trabalho, avaliou-se a função destes nervos na manutenção da histologia da glândula. Dessa forma, os nervos aferentes e eferentes de ratos machos foram seccionados As regiões ventral e dorsolateral da próstata foram processadas para histologia. Os resultados mostraram que a transecção aferente afeta a histologia da próstata. A área alveolar diminuiu e aumentou na próstata dorsal e dorsolateral, respectivamente. A altura da célula epitelial aumentou em ambas as regiões. A desenervação eferente produziu alterações dramáticas na glândula prostática. O tecido perdeu a sua configuração e o epitélio tornou-se difuso e quase desapareceu. Assim, os nervos aferentes são responsáveis por processos espinhais que pertencem ao controle trófico da próstata, ativando sua inervação autonômica. Dessa forma, nossos dados sugerem que a inervação parece ser sinérgica com os hormônios para a manutenção saudável da próstata. Assim, sugere-se que algumas patologias prostáticas poderiam ser ocasionadas devido a falhas nas vias neurais autonômicas que regulam esta glândula.

Intrinsic heart rate after infusion of angiotensin II in rats with sino-aortic deafferentation

We investigated the effect of the infusion of angiotensin II on intrinsic heart rate in rats with sin-aortic deafferentation. Sino-aortic deafferented (SAD) rats studied 48 h after surgery presented significant tachycardia when compared with sham-operated rats (425 ñ 16 vs 338 ñ6 bpm), but no change in intrinsic heart rate (369 ñ vs 369 ñ 11 bpm). Infusion of angiotensin II into the SAD group 48 h after deafferentation did not produce an additional increase in heart rate (423 ñ 16 vs 426 ñ 16 bpm) or a change in intrinsic heart rate (369 ñ 11 vs 369 ñ 9 bpm) when compared with sham-operated rats submitted to saline infusion. Intravenous (iv) infusion of angiotensin II into sham- operated rats produced a significant increase in both heart rat (381 ñ 12 vs 338 ñ 6 bpm) and intrinsic heart rate (427 ñ vs 369 ñ 11 bpm). These data indicate that a) tachycardia after SAD is not associated with an increase in intrinsic heart rate, b) in sham-operated rats, the tachycardia occuring after angiotensin II infusion is associated with an increase in intrinsic heart rate, and c) angiotensin II infusion does not alter the intrinsic heartrate of rats tested 48 h after sino-aortic deafferentation. We conclude that the increase in intrinsic heart rate caused by angiotensin II in conscious rats depends on the integrity of the baroreceptor reflex

Arterial pressure responses to adrenoceptor antagonism in rats with sino-aortic deafferentation

1. The effect of sequential alpha and beta adrenoceptor blockade on mean arterial pressure (MAP) and arterial presure lability (APL) was studied 3 days after sino-aortic deafferentation (SAD) in rats. 2. Prazosin, an alpha-1 adrenoceptor blocker, injected iv (1 mg/Kg) into SAD 3 days after surgery produced a significant fall in MAP (-61 vs - 21 mmHg) and APL (-7 vs 0mmHg) when compared with sham-operated rats. 3. Propranolol, a beta-1 and -2 adrenoceptor blocker, injected iv (1 mg/Kg) after prazosin into SAD rats (3 days) produced a significant increase in MAP (+37 vs + 5mmHg) and APL (+4 vs 0mmHf) when compared with sham-operated rats. 4. Prazosin injected iv (1 mg/Kg) into SAD rats 15 days after surgery produced smaller changes in MAP rthan observed in rats 3 days after SAD but a significant fall in MAP (-35 vs -13mmHg) when compared with sham-operated rats. At this phase of SAD, no changes in APL were observed after prazosin. 5. Propranolol injected iv (1 mg/Kg) after prozosin into SAD and sham-operated rats (15 days) produced no changes in MAP and APL. 6. Prazosin injected into SAD rats (3 and 15 days) with previous adrenal demedullation produced falls in MAP and APL similar to those observed in SAD rats with intact adrenals. 7. In contrast to SAD rats with intact adrenals, propranolol injected after prozosin into SAD rats (3 days) with previous adrenal demedullation produced no increase in MAP. 8. These results suggest that a) alpha-1 adrenoceptors are directly involved in MAP maintenance in SAD rats 3 and 15 days after surgery; b) weeks after SAD, compensatory reflex mechanisms may be acting to reduce the fall in MAP produced by prazosin; c) alpha-1 adrenoceptores are not directly involved in APL generation; d) APL is related to the activation of beta adrenoceptors by endogenous epinephrine release