Hypertension and the Eye... Pathogenesis?

In my last article on "Hypertension and the Eye... What the primary Eye care Optometrist Should know.", I pointed out some ocular consequences of this systemic condition viz: Retinopathies, changes in refractive status as the eye of the chronic hypertension patient, choroidal degenerative changes and general changes in ocular vascular supplies with an increasing affinity for low vision in subjects.
The ocular effect of hypertension, especially on the collagen matrix making up the most vulnerable portions of the eyes, is not really new to eye care. The ocular blood vessels, the choroidal and retinal surfaces, the crystalline lens, even the jelly vitreous humor are all kept in shape by the collagen matrix that gives structural rigidity to this delicate organ-the eye- and ironically becomes the main connecting tissue to be weakened by hypertension or so I think.
Can the pathogenesis of ocular manifestation of hypertension be explainable by the weakening of the collagen matrix of the eyes? What is the relationship between hypertension disease degenerative condition and collagen matrix weakening effect? Are we saying that maintaining the integrity of the ocular collagen connective tissue matrix is one of the means to manage ocular manifestation of hypertension? What does it mean to have a weakened collagen matrix?
Lets take a detour.
Elastin and collagen are the most important components of blood vessels extra-cellular matrix, giving the necessary strength and elasticity to blood vessels, including the capillaries. The blood vessels- veins, venules, capillaries, arterioles and arteries-characteristically presents with the tunica adventitia, tunica media and tunica intima with their modifications based on function and location.
The capillaries contain no tunica media (the structure the reinforces vascular tensile strength) but has modified endothelium (tunica intima) and oftentimes its tunica adventitia is modified into a base membrane.

In hypertension, arteriolosclerosis and arteriosclerosis collagen, back bone of the vascular connective tissue, is always the victim and the much hyped degenerations associated with this condition (Hypertension) becomes the consequence. Insult on the surrounding vascular endothelium leads to increasing production of collagen in the process of fibrogenesis. Suddenly there is increased proliferation of fibrocytes and subsequent formation of fibroblasts resulting in increase in connective tissue activity, perhaps to ameliorate the insult of the arterial blood pressure/resistance on the vessel! The proliferated formation of new collagen connective tissues in this instance does not follow the normal pattern and hence a less structurally similar network of collagen bundle results to a vulnerable and weakened structure.

Connective tissue (CT) is a kind of biological tissue that supports, connects, or separates different types of tissues and organs of the body. (Wikipedia). Collagen and its extra cellular matrix provides such function in the blood vessels and in short could be seen as a bag or container of less "rigid" body tissues. In supporting the tissues and organs of the body, the connective tissue is known to provide some kind of defense to its content. Eg Fibrosis (a kind of supporting function of the connective tissue) is caused by a series of events, triggered by chronic injury. These events include:
1) immediate damage to the epithelial/endothelial barrier;
2) release of TGF-b1, the major fibrogenic cytokine;
3) recruitment of inflammatory cells;
4) induction of reactive oxygen species (ROS);
5) activation of collagen producing cells;
6) matrix activation of myofibroblasts; and,
7) in the absence of continuous injury, reversal of fibrosis.
(TATIANA KISSELEVA AND DAVID A. BRENNER. Mechanism of Fibrogenesis.Experimental Biology and Medicine 2008, 233:109-122.).

The fibrosis process as outlined above is similar in almost all the structures having collagenous connective tissues but different organs' connective tissues effect different structural adjustments leading to compromised intra-tissue coherence and hence the disintegration/degenerations in the susceptible vessels, tissues, organs etc!

In rats, AKIRA OOSHIMA et al in "Increased Collagen Synthesis in Blood Vessels of Hypertensive Rats and Its Reversal by Antihypertensive Agents. Vol.71,No.8,pp.3019-3023,August1974.", observed increased collagen synthesis and thickening in the aorta, mensentric arteries and to a lesser extent in the heart. They observed that the increased synthesis of collagen is a direct result of the effect of hypertension on these structures.
In end vessels and in very tiny blood capillaries, arteriolosclerosis is induced and its many consequence like vascular rupture in advanced retinopathies, choroidopathies, maculopathies, aneurysms and even breakdown in collagen type ll of the vitreous humor, the collapse of the lamina cribosa, and many more such sclerosis in the vulnerable eye, kidney,heart, distal part of the arms, limbs or cerebral contents!

Little wonder we are faced with multiple ocular signs of ocular manifestations of hypertension, not only that the eyes are reinforced by the collagen network- the cornea has type l collagen, collagen present in the vitreous are types II,XI,VI and IX; the sclera is composed of type l and type lll collagen, the retina is composed of types I, ll, lll, lV, V, VI and XVIII, the retinal vessel is composed of collagen types I, III, IV, V, VI, and XVIII, the choroid is composed of type l, lV and type XVlll, lens capsule collagen consisted mainly of type IV collagen etc- it is almost exclusively held in place by this connective tissue. Varying degrees of injuries are inflicted to these connective tissues in chronic hypertension.

As primary eye care practitioners we are therefore expected to be in the fore-front of promoting preventive health care maneuvers that will reduce the incidence of this, often irreversible, structural changes- anatomically and physiologically- in the ocular plexus. We must ensure that our patients susceptible to chronic and/or acute insult cum injury are kept from harms way by ensuring any of the underlying causes are addressed as early as possible and we should work closely with GPs to ensure that the patients adhere strictly to their medications and check ups! Ones their underlying systemic cause is removed normalcy returns in collagen synthesis and other tissue functions ameliorated. Even if the underlying cause is not the entire system, it is advised that the condition be isolated, if it is within our scope of practice, or referred to a specialist in a co-managed process.
Finally, chronic effect of hypertension can be sight threatening and early detection and management is the best option, we are therefore required to always remind our hypertensive patients of this with the aim of healthy vision of the subjects.
Long live Naija Optometry.
We can do better.
Thanks.
Dr Ezebuiroh Okwudiri Victor.
This article is exclusively my opinion.