The maintenance of ionic concentration gradients across the membrane. The maintenance of these concentration gradients requires the expenditure of energy (ATP hydrolysis) coupled with ionic pumps. Consider for a moment the concentration gradients for Na+ and K+. Whenever an action potential is generated, Na+ enters the cell and K+ leaves the cell. While the number of ions moving across the sarcolemmal membrane in a single action potential is very small relative to the total number of ions, after many action potentials are generated, there would occur a significant change in the extracellular and intracellular concentration of these ions. To prevent this from occurring (i.e., to maintain the concentration gradients for Na+ and K+), there is located on the sarcolemma an energy dependent (ATP-dependent) pump system (Na+/K+-ATPase) that pumps Na+ out of the cell and K+ into the cell. Normal operation of this pump is essential for the maintenance of Na+ and K+ concentrations across the membrane. If this pump stops working (as occurs under anoxic conditions when ATP is lost), or if the activity of the pump is inhibited (as occurs with cardiac glycosides such as digitalis), Na+ accumulates within the cell and intracellular K+ falls. This causes depolarization of the resting membrane potential.  Furthermore, it is important to note that this pump is electrogenic in nature because it extrudes 3 Na+ for every 2 K+ entering the cell.  By pumping more positive changes out of the cell than into the cell, the pump activity creates a negative potential within the cell.  This potential may be up to -10 mV.  Inhibition of this pump, therefore, causes depolarization resulting not only from changes in Na+ and K+ concentration gradients, but also from the loss of an electrogenic component of the membrane potential.  
Because Ca++ enters the cell during action potentials, it is necessary to maintain its concentrations gradients.  This is accomplished by Ca++ pumps and exchangers on the membrane.

Neurohumoral mechanism maintaining normal cardiac output and blood pressure

Acute haemorrhage :

 1) Rapidly acting pressure control mechanisms; to return blood pressure to  physiological levels. All are nervous mechanisms:
  i) Baroreceptor
  ii) Chemoreceptor
  iii) CNS ischaemic response

 2) Long term mechanisms for arterial pressure regulation; to return blood  volume to normal levels. Essentially involves kidney control via several  hormonal mechanisms:
  i) Renin — Angiotensin
  ii) Aldosterone