Just to add onto what others have said, it depends on what's causing the blood pressure to rise. SNS constricts arteries towards certain organs (including kidney), so that other tissues that need it (for "fight or flight" response) are able to retain the much needed blood. This includes the heart, the brain, and skeletal muscle. By constricting arteries towards other organs, this increases venous return and cardiac output (indirectly) which increases systemic pressure. Also, the restriction of various arteries increases resistance which also facilitates an increase in pressure. Decreases blood filtration in the kidney occurs because less blood is directed towards the kidney.
Other factors play a role in blood pressure as well. Think about someone in a car accident who is losing a tremendous amount of blood. Their blood pressure will drop immensely. Barocepters on the heart signal the hypothalamus to increase release of ADH. ADH acts on the collecting duct in the kidney to increase venous return by reabsorption of water.
Think about someone whose been stuck on a desert for sometime (very low water intake). These individuals have blood that is hyperosmotic and therefore very low blood pressure (more solute, too little fluid). Normal blood has an osmolarity of 300 mOsm (above that is considered hypertonic). Receptors in the hypothalamus (osmoreceptors), recognize this and also stimulate ADH release (same function as above). At the same time, the renin-angiotensin-aldosterone pathway is activated. The enzyme renin is released by juxtaglomerular cells in the kidney upon stimulation of macula densa cells (specialized cells that monitor sodium levels and blood flow). Renin activates angiotensinogen to angiotensin I. Angiotensin I is activated b ACE (released by lungs) to Angiotensin II; AII is a powerful vasoconstrictor and increases blood pressure by vasoconstriction. At the same time it constricts both the afferent and efferent arteriole, although the efferent to a greater degree. (This might seem counter intuitive since constriction of efferent increases GFR and increases filtrate output but I believe this is a feedback mech; I never heard a proper explanation). AII also activates aldosterone release in the adrenal cortex. Aldosterone increases sodium reabsorption which ultimately results in increased water reabsorption, also allowing increased blood pressure.
Still, other factors can influence pressure. On the other side of the spectrum, people who have high blood pressure for sometime cause the cardiac cells of the heart to stretch. This stretching releases ANP which acts on the kidneys to increase sodium excretion and thereby reduce reabsorption of water.
I think I have that right, but if anyone sees anything erroneous please let me know.
