Cardiac muscle is striated similar to skeletal muscle but with one major difference. Cardiac muscle fibres are all interconnected to one another, forming a mesh like structure. This enables contraction of one muscle fibre to be felt by others and therefore this contraction is spread to all the muscle fibres enabling the cardiac muscle fibres to contract and function as a syncytitium. Also the thing that enables the contractions to be transmitted to the other muscle fibres is the structural connections between the cardiac muscle fibres known as intercalated discs. Structurally these have three main components: Fascia adherens, macula adherens and a gap junction. The FA is responsible for transmitting the mechanical contractile forces associated with the cytoskeletal elements of the muscle fibre. The macula adherens is responsible for providing strong attachment between the cardiac muscle fibres and therefore maintain the integrity of the mesh work arrangement. The gap junctions provides for electrical continuity between the cardiac muscle cells, therefore enabling the action potentials to be transmitted across the whole myocardium.  

The action potential initiated in a cardiac muscle cell is due to its membrane potential being altered causing a depolarisation similar to a skeletal muscle. The sudden opening of Na+ channels causes an influx of Na ions into the cell and therefore reduces the membrane potential. This causes the sudden opening of calcium channels are the membrane threshold potential for this gates to be opened has been reached, and as a result increased amounts of Ca+ ions enter the cell. This enables them to participate in active cross bridges and therefore enable the muscle fibres to stretch. The entry of calcium ions provides a prolonged phase of depolarisation and this is known as the plateau phase. 

When depolarisation is complete, repolarisation of the membrane is due to closing of ca channels and opening of the slow potassium channels. The membrane potential is restored and the whole process begins again when the heart contracts again. The internal structure of the cardiac muscle cells is different from that of skeletal muscle fibres. The muscle fibre does not have an extensive SeR and the t-Tubules are wider compared to those of skeletal muscle fibres.  

Major Points: Meshwork arrangement & functional syncytium, Intercalated discs & three types & identify and elaborate , How does depolarisation occur & elaborate , Repolarisation & elaborate, Internal structure of cell & seR, and t-Tubules, no terminal cisternae evident

1999_2^nd semester_Q2_Part_B 

There are a number of mechanisms that control the tone of smooth muscle surrounding blood vessels. Smooth muscle surrounding arterioles are richly innervated by the sympathetic fibres from the autonomic nervous system. These fibres are normally postganglionic fibres which release noradrenaline. The smooth muscle plasma membranes have a rich supply of alpha adrenergic receptors and as a result when noradrenaline binds to these receptors, vasoconstriction results and therefore the arterial blood pressure increases due to the increase in total peripheral resistance. Noradrenaline binding to non-innervated B2 receptors on skeletal and cardiac muscle causes vasodilation.

The arterioles are always partially constricted due to the rich innervation of the vascular smooth muscle. This is called vascular tone. This is similar to skeletal muscles always being partially contracted called muscle tone.

Sympathetic fibres innervating blood vessels supplying skeletal and cardiac muscle release acetylecholine from their terminals and this binds to the smooth muscle have a vasodilator effect. Also smooth muscle is controlled by the amount of nitric oxide present as this is a potent vasodilator.

An increase in smooth muscle tone, constricts the blood vessel decrease its luminal size and therefore increases resistance and pressure. This reduces blood flow to the areas affected, and can also function to shunt blood to areas requiring more immediate supply of blood.

Major Points: Identify rich Innervation, Postganglionic fibres releasing noradrenaline bind with apha adrenergic receptors on smooth muscle to cause vasoconstriction , Also adrenaline released from the adrenal medulla binds to non - innervated b2 receptors to cause vasodilation, Vascular tone & smooth muscle associated with arterioles is partially constricted. Vasodilation due to nitric oxide & potent vasodilator , Acetylcholine binding to receptors on the smooth muscle surround BV’s of the skeletal tissues and cardiac muscle produce vasodilation. Increase in smooth muscle tone & increases resistance & increases pressure & therefore decreases blood flow & functional significance in fight or flight response.