Autoregulation

[7] This is in contrast to heterometric regulation, governed by the Frank-Starling law, where increased ventricular filling stretches sarcomeres, optimizing actin-myosin filament overlap to enhance cross-bridge formation.

This process, known as 'myofilament length-dependent activation', includes structural changes in myosin, involving a transition from rested to contraction-ready states.

[10] This shift increases the number of myosin heads available for actin binding, amplifying myocardial force production.

Additional mechanisms, such as increased calcium sensitivity of myofilaments, further enhance contractile strength and stroke volume.

[11] Since the heart is a very aerobic organ, needing oxygen for the efficient production of ATP & Creatine Phosphate from fatty acids (and to a smaller extent, glucose & very little lactate), the coronary circulation is auto regulated so that the heart receives the right flow of blood & hence sufficient supply of oxygen.

The sodium chloride levels in the urinary filtrate are sensed by the macula densa cells at the end of the ascending limb.

Further increase in sodium concentration leads to the release of nitric oxide, a vasodilating substance, to prevent excessive vasoconstriction.