1.) What do you understand by the term 'endothelium-dependent' vasodilation?

Endothelium-dependent vasodilators act by increasing intracellular calcium levels in the endothelium cells leading to the synthesis of NO. NO diffuses to the vascular smooth muscle leading to vaso-relaxation. 

2.) When we talk about NOS enzyme, what is meant by constitutive and inducible enzymes and what are the pathalogical and physiological implications thereof?

NOS1 and NOS3 are commonly associated constitutive expression. Their activity is calcium dependent and requires interaction between the NOS enzyme and calmodulin-bound calcium to facilitate the catalysis of L-arginine and production of NO. 

Inducible expression of NOS has long been associated with immunological function. Immune cells use NO often in conjunction with reactive oxygen intermediates to kill pathogens and cancer cells. NOS2 is minimally expressed or is not abundant intracellularly in macrophages unless immune related stimulation and gene transcription occurs. Once transcribed NOS2 has a high affinity binding site for calmodulin and can function in a calcium-independent manner suggesting that at any time it is expressed it is likely to be active.

3.) Explain how NO contributes to the fatal pathology of septic shock.

Endotoxin components from the bacterial wall along with endogenously generated tumor necrosis factor-α and other cytokines induce synthesis of iNOS in macrophages, neutrophils and T-cells as well as hepatocytes, smooth muscle cells, endothelial cells and fibroblasts. The widespread generation of NO results in exaggerated hypotension, shock and some cases death.

4.) Which autacoids mechanism of action depends on effects on the guanylyl cyclase-cGMP system?

Nitric Oxide

5.) NO may be toxic to the cell. Which mechanism is available to the body to counter this detrimental effect of NO?

NOS enzyme inhibition majority of these being arginine analogs that bind to the NOS arginine binding site.

6.) Name a way in which NO can act as a pro-inflammatory. Give examples of where it will have advantages or disadvantages.

NO can act as a pro-inflammatory in the host immune response and in inflammation. Host response to infection or injury involves recruitments of leukocytes and release of inflammatory mediators like tumor necrosis factor and interleukin-1. This leads to a marked increase in iNOS levels and activity in leukocytes fibroblasts and other cell types.

However in both acute and chronic inflammatory conditions, prolonged or excessive NO production may exacerbate tissue injury. 

7.) In which possible neurological and psychiatric diseases is NO involved?

Stroke, amyotrophic lateral sclerosis and Parkinson's disease.