Answer:
The autonomic nervous system is the main neural regulator of circulation and blood pressure in the short term and beat by beat and exerts its function through various reflexes that regulate vasomotor tone, heart rate and cardiac output. At the renal level, the renin–angiotensin–aldosterone system is possibly the most important in the maintenance of arterial homeostasis.
Explanation:
Blood pressure is regulated by a series of interrelated autonomic systems and humoral reflexes, which continually adjust the determining elements of the system (heart rate, stroke volume, total peripheral resistance and circulating volume).The effective circulating volume is controlled by a series of reflex systems, which obtain information about the perfusion pressure (baroreceptors in the carotid bulb and aortic arch), plasma osmolarity (hypothalamus) and urinary sodium (distal tubule).The kidney has its own self-regulatory mechanisms. The reduction in renal blood flow is detected at the level of the mesangial cells of the juxtaglomerular apparatus, starting the renin-angiotensin system. The increase in angiotensin II produces on the one hand local vasoconstriction, and on the other hand stimulates the production of aldosterone by the adrenal cortex with the consequent tubular reabsorption of sodium and water.Antidiuretic hormone or vasopressin (released from the hypothalamus by stimulation of arterial baroreceptors and also by stimulation of angiotensin II) also acts at the renal level, which acts as a powerful and water-saving vasoconstrictor in the distal tubule.
Answer:
(A) It prevents electron flow from the iron-sulfur centers in complex 1 to the ubiquinone. Due to reduction in electron transfer rate, there is a decrease in the production of ATP which is dangerous for some insects and fish over time.
(B) It also prevents electron flow from cytochrome b to cytochrome c1 at the complex III which leads to QH2 accumulation. If oxidized Q is not present, these is alteration of electron flow and the production of ATP is altered.
(C) Rotenone only prevent electron transfer into the chain at Complex 1 but it does not affect electron transfer at Complex II. Although there is slow ETC, it does not stop completely. However, Antimycin A prevents the oxidation of QH2, the final electron acceptor crom complex I and complex II. Thereby, stopping the production of both ETC and ATP. It can be concluded that antimycin A is a more potent poison.
Explanation:
Rotenone prevents electron flow from the iron-sulfur centers in complex 1 to the ubiquinone. Due to a reduction in electron transfer rate, there is a decrease in the production of ATP which is dangerous for some insects and fish over time. Antimycin A also prevents electron flow from cytochrome b to cytochrome c1 at the complex III which leads to QH2 accumulation. If oxidized Q is not present, there is an alteration of electron flow and the production of ATP is altered. Antimycin A is more potent than rotenone.
Because most waste produced in the cell is toxic when it accumulates.
Hope this helps!
The cytoplasm fills the cell and is surrounded by the cell membrane. :)
